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rabbit anti cyclin a2 ccna2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti cyclin a2 ccna2
    Post-mitotic iPSC-derived motor neurons from C9orf72 carriers aberrantly enter cell-cycle (A) Representative images of control and C9orf72 motor neuron cultures. Scale bars, 100 μm. (B–C) mRNA levels of Ki67 and GMNN at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (D) Representative western blot images of GMNN and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (E–F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from control (lines: 35L5, 35L11, and 37L20) and C9orf72 (lines: 16L14, 40L3, and 42L11). (G) Percentage of neurons in S-phase from controls and C9orf72 neurons. (H and I) mRNA levels of <t>CCNA2</t> and CCNB2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (J and K) mRNA levels of CDK2 and CDK4 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (L) Representative western blot images of CCNA2 and GAPDH and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (M) Representative western blot images of CDK4 and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. Data are presented as mean ± SEM (B–D, G–M). Data presented in (B–D) is from 3 control and 3 C9orf72 iPSC iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. Data presented in (G) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05. Data presented in (H–K) 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05 and ∗∗ p < 0.01. Data presented in (L and M) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ∗ p < 0.05. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.
    Rabbit Anti Cyclin A2 Ccna2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 69 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+cyclin+a2+ccna2/Cyclin+A2+XP+Rabbit+mAb/pmc12856326-3-0-5
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    Images

    1) Product Images from "Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD"

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD

    Journal: iScience

    doi: 10.1016/j.isci.2025.114596

    Post-mitotic iPSC-derived motor neurons from C9orf72 carriers aberrantly enter cell-cycle (A) Representative images of control and C9orf72 motor neuron cultures. Scale bars, 100 μm. (B–C) mRNA levels of Ki67 and GMNN at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (D) Representative western blot images of GMNN and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (E–F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from control (lines: 35L5, 35L11, and 37L20) and C9orf72 (lines: 16L14, 40L3, and 42L11). (G) Percentage of neurons in S-phase from controls and C9orf72 neurons. (H and I) mRNA levels of CCNA2 and CCNB2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (J and K) mRNA levels of CDK2 and CDK4 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (L) Representative western blot images of CCNA2 and GAPDH and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (M) Representative western blot images of CDK4 and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. Data are presented as mean ± SEM (B–D, G–M). Data presented in (B–D) is from 3 control and 3 C9orf72 iPSC iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. Data presented in (G) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05. Data presented in (H–K) 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05 and ∗∗ p < 0.01. Data presented in (L and M) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ∗ p < 0.05. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.
    Figure Legend Snippet: Post-mitotic iPSC-derived motor neurons from C9orf72 carriers aberrantly enter cell-cycle (A) Representative images of control and C9orf72 motor neuron cultures. Scale bars, 100 μm. (B–C) mRNA levels of Ki67 and GMNN at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (D) Representative western blot images of GMNN and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (E–F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from control (lines: 35L5, 35L11, and 37L20) and C9orf72 (lines: 16L14, 40L3, and 42L11). (G) Percentage of neurons in S-phase from controls and C9orf72 neurons. (H and I) mRNA levels of CCNA2 and CCNB2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (J and K) mRNA levels of CDK2 and CDK4 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (L) Representative western blot images of CCNA2 and GAPDH and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (M) Representative western blot images of CDK4 and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. Data are presented as mean ± SEM (B–D, G–M). Data presented in (B–D) is from 3 control and 3 C9orf72 iPSC iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. Data presented in (G) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05. Data presented in (H–K) 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05 and ∗∗ p < 0.01. Data presented in (L and M) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ∗ p < 0.05. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

    Techniques Used: Derivative Assay, Control, Western Blot, Flow Cytometry, Staining, Two Tailed Test, Membrane

    Poly (GR) induces an increase in cyclins and CDKs levels (A) Schematic representation of the CRISPR/Cas9 strategy to generate C9orf72 homozygous and heterozygous lines from a healthy control line. (B) Generation of C9orf72 heterozygous and homozygous knockout iPSC lines by CRISPR Cas9. (C) Representative western blot image of C9orf72 protein levels in homozygous (line 3) and heterozygous (line 8) knockout lines by CRISPR Cas9. (D–G) mRNA levels of Ki67, GMNN, CDK4, and CCNA2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (H) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GR). Scale bars, 200 μm. (I and J) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (K) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GP). Scale bars, 200 μm. (L and M) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (N) Representative western blot image of control iPSC-derived neurons treated with Poly (GR) and poly (GP). (O and P) Quantification of protein levels of CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR) and poly (GP). Data are presented as mean ± SEM (D–G, I and J, L and M, O and P). Data presented in (D–G) is from 3 independent differentiation experiments of a control iPSC line (parental line) and one C9orf72 heterozygous and one homozygous knockout line. Two-tailed t test with Welch’s correction was applied. ns, not significant. Data in (I and J, L and M) is from 3 control iPSC lines treated with DPRs from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. Data in (O and P) is from 3 control iPSC lines treated with DPRs from 2 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.
    Figure Legend Snippet: Poly (GR) induces an increase in cyclins and CDKs levels (A) Schematic representation of the CRISPR/Cas9 strategy to generate C9orf72 homozygous and heterozygous lines from a healthy control line. (B) Generation of C9orf72 heterozygous and homozygous knockout iPSC lines by CRISPR Cas9. (C) Representative western blot image of C9orf72 protein levels in homozygous (line 3) and heterozygous (line 8) knockout lines by CRISPR Cas9. (D–G) mRNA levels of Ki67, GMNN, CDK4, and CCNA2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (H) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GR). Scale bars, 200 μm. (I and J) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (K) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GP). Scale bars, 200 μm. (L and M) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (N) Representative western blot image of control iPSC-derived neurons treated with Poly (GR) and poly (GP). (O and P) Quantification of protein levels of CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR) and poly (GP). Data are presented as mean ± SEM (D–G, I and J, L and M, O and P). Data presented in (D–G) is from 3 independent differentiation experiments of a control iPSC line (parental line) and one C9orf72 heterozygous and one homozygous knockout line. Two-tailed t test with Welch’s correction was applied. ns, not significant. Data in (I and J, L and M) is from 3 control iPSC lines treated with DPRs from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. Data in (O and P) is from 3 control iPSC lines treated with DPRs from 2 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

    Techniques Used: CRISPR, Control, Knock-Out, Western Blot, Derivative Assay, Immunostaining, Two Tailed Test, Membrane

    CDK4/6 inhibitor Palbociclib (PD33002291) prevents cell-cycle reentry in iPSC-derived motor neuron from C9orf72 carriers (A and B) Western blot and quantification of protein levels of phosphorylated RB and topoisomerase II α (TopoII) in 2-month-old iPSC-derived motor neurons from C9orf72 carriers treated with Palbociclib 1 and 5 μM. (C–E) mRNA levels of Ki67 and CCNA2 and CDK1 in 2-month-old C9orf72 iPSC-derived motor neurons treated with Palbociclib 5 μM. (F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from controls, C9orf72 and C9orf72 neurons treated with Palbociclib 5 μM. (G) Quantification of the percentage of C9orf72 iPSC-derived motor neurons in S-phase. Data are presented as mean ± SEM (A–E, G). Data presented in (A and B) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 treated with Palbociclib 1 and 5 μM from 2 differentiation experiments, one-way ANOVA with Newman-Keuls post hoc test was applied ∗ p < 0.05.∗∗ p < 0.01 and ∗∗∗ p < 0.001. Data presented in (C–E) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 neurons with Palbociclib 5 μM from 2 differentiation experiments. Two-tailed t test with Welch’s correction was applied ∗ p < 0.05 and ∗∗ p < 0.01. Data in (G) is from iPSC-derived neurons from 3 controls, 3 C9orf72 , and 3 C9orf72 treated with Palbociclib from 1 differentiation experiment, one-way ANOVA with Newman-Keuls post hoc test was applied ∗∗ p < 0.01. See also .
    Figure Legend Snippet: CDK4/6 inhibitor Palbociclib (PD33002291) prevents cell-cycle reentry in iPSC-derived motor neuron from C9orf72 carriers (A and B) Western blot and quantification of protein levels of phosphorylated RB and topoisomerase II α (TopoII) in 2-month-old iPSC-derived motor neurons from C9orf72 carriers treated with Palbociclib 1 and 5 μM. (C–E) mRNA levels of Ki67 and CCNA2 and CDK1 in 2-month-old C9orf72 iPSC-derived motor neurons treated with Palbociclib 5 μM. (F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from controls, C9orf72 and C9orf72 neurons treated with Palbociclib 5 μM. (G) Quantification of the percentage of C9orf72 iPSC-derived motor neurons in S-phase. Data are presented as mean ± SEM (A–E, G). Data presented in (A and B) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 treated with Palbociclib 1 and 5 μM from 2 differentiation experiments, one-way ANOVA with Newman-Keuls post hoc test was applied ∗ p < 0.05.∗∗ p < 0.01 and ∗∗∗ p < 0.001. Data presented in (C–E) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 neurons with Palbociclib 5 μM from 2 differentiation experiments. Two-tailed t test with Welch’s correction was applied ∗ p < 0.05 and ∗∗ p < 0.01. Data in (G) is from iPSC-derived neurons from 3 controls, 3 C9orf72 , and 3 C9orf72 treated with Palbociclib from 1 differentiation experiment, one-way ANOVA with Newman-Keuls post hoc test was applied ∗∗ p < 0.01. See also .

    Techniques Used: Derivative Assay, Western Blot, Flow Cytometry, Staining, Two Tailed Test

    Related Articles

    Derivative Assay:

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Control:

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Western Blot:

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Flow Cytometry:

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Staining:

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Two Tailed Test:

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Membrane:

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    CRISPR:

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Knock-Out:

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Immunostaining:

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.



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    Expression of <t>CCNA2</t> in CRC and its effect on biological behavior of CRC cells . A , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by immunohistochemistry assay. B , the mRNA expressions of CCNA2 were detected in paracancerous and CRC tissues by quantitative PCR (qPCR) assay. C , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by Western blotting. D , the protein expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by Western blotting. E , the mRNA expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by qPCR assay. F , the interference efficiency of knockdown CCNA2 expression in the HCT116 and HT29 stable cell lines was evaluated by Western blotting. G , CCK-8 assay showed that knockdown of CCNA2 expression inhibited the proliferation of HT29 and HCT116 cells. H , wound scratch assay demonstrated that hat knockdown of CCNA2 expression inhibited the migration of HT29 and HCT116 cells. I , Transwell assay revealed that knockdown of CCNA2 expression inhibited the invasion of HT29 and HCT116 cells. J , flow cytometry assay indicated that knockdown of CCNA2 expression induced the apoptosis of HT29 and HCT116 cells. K – L , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in HT29 and HCT116 cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.
    Antibodies Ccna2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ccna2  (ABclonal Biotechnology)
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    A Schematic representation of xenograft tumor of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel, and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. B The weight of xenograft tumor of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel, and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. C The volume of xenograft tumor of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel, and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. D The immunohistochemical staining of IGF2BP3, c-Myc, and Ki-67 of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. Scale bar, 20 μm. E Venn analysis based on c-Myc-targeted genes in GSEA, up-regulated genes in RNA-seq of paclitaxel-resistant Ishikawa cells, and down-regulated genes in RNA-seq of IGF2BP3 knockdown Ishikawa cells. F The immunohistochemical staining of <t>CCNA2</t> and CCT2 of of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. Scale bar, 20 μm. G Molecular mechanism of IGF2BP3/SPOP/c-Myc loop mediated paclitaxel resistance (Created in BioRender. Zhang, H. (2025) https://BioRender.com/bjcmb9j , Agreement number: DY282PE8YM). Scale bar, 20 μm. Data are shown as mean ± SD ( n ≥ 3). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
    Ccna2, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    cyclin a2 ccna2  (Cell Signaling Technology Inc)
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    Cell cycle regulator proteins expression in different CTR groups. A–H the expression of <t>CCNA2,</t> CCNB1, CCND1, TP53, P16, P21, TOP2A, and pRb in lung adenocarcinoma with different CTR. CTR, consolidation-to-tumour ratio
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    Image Search Results


    Post-mitotic iPSC-derived motor neurons from C9orf72 carriers aberrantly enter cell-cycle (A) Representative images of control and C9orf72 motor neuron cultures. Scale bars, 100 μm. (B–C) mRNA levels of Ki67 and GMNN at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (D) Representative western blot images of GMNN and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (E–F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from control (lines: 35L5, 35L11, and 37L20) and C9orf72 (lines: 16L14, 40L3, and 42L11). (G) Percentage of neurons in S-phase from controls and C9orf72 neurons. (H and I) mRNA levels of CCNA2 and CCNB2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (J and K) mRNA levels of CDK2 and CDK4 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (L) Representative western blot images of CCNA2 and GAPDH and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (M) Representative western blot images of CDK4 and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. Data are presented as mean ± SEM (B–D, G–M). Data presented in (B–D) is from 3 control and 3 C9orf72 iPSC iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. Data presented in (G) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05. Data presented in (H–K) 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05 and ∗∗ p < 0.01. Data presented in (L and M) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ∗ p < 0.05. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

    Journal: iScience

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD

    doi: 10.1016/j.isci.2025.114596

    Figure Lengend Snippet: Post-mitotic iPSC-derived motor neurons from C9orf72 carriers aberrantly enter cell-cycle (A) Representative images of control and C9orf72 motor neuron cultures. Scale bars, 100 μm. (B–C) mRNA levels of Ki67 and GMNN at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (D) Representative western blot images of GMNN and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (E–F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from control (lines: 35L5, 35L11, and 37L20) and C9orf72 (lines: 16L14, 40L3, and 42L11). (G) Percentage of neurons in S-phase from controls and C9orf72 neurons. (H and I) mRNA levels of CCNA2 and CCNB2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (J and K) mRNA levels of CDK2 and CDK4 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (L) Representative western blot images of CCNA2 and GAPDH and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (M) Representative western blot images of CDK4 and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. Data are presented as mean ± SEM (B–D, G–M). Data presented in (B–D) is from 3 control and 3 C9orf72 iPSC iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. Data presented in (G) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05. Data presented in (H–K) 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05 and ∗∗ p < 0.01. Data presented in (L and M) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ∗ p < 0.05. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Techniques: Derivative Assay, Control, Western Blot, Flow Cytometry, Staining, Two Tailed Test, Membrane

    Poly (GR) induces an increase in cyclins and CDKs levels (A) Schematic representation of the CRISPR/Cas9 strategy to generate C9orf72 homozygous and heterozygous lines from a healthy control line. (B) Generation of C9orf72 heterozygous and homozygous knockout iPSC lines by CRISPR Cas9. (C) Representative western blot image of C9orf72 protein levels in homozygous (line 3) and heterozygous (line 8) knockout lines by CRISPR Cas9. (D–G) mRNA levels of Ki67, GMNN, CDK4, and CCNA2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (H) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GR). Scale bars, 200 μm. (I and J) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (K) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GP). Scale bars, 200 μm. (L and M) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (N) Representative western blot image of control iPSC-derived neurons treated with Poly (GR) and poly (GP). (O and P) Quantification of protein levels of CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR) and poly (GP). Data are presented as mean ± SEM (D–G, I and J, L and M, O and P). Data presented in (D–G) is from 3 independent differentiation experiments of a control iPSC line (parental line) and one C9orf72 heterozygous and one homozygous knockout line. Two-tailed t test with Welch’s correction was applied. ns, not significant. Data in (I and J, L and M) is from 3 control iPSC lines treated with DPRs from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. Data in (O and P) is from 3 control iPSC lines treated with DPRs from 2 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

    Journal: iScience

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD

    doi: 10.1016/j.isci.2025.114596

    Figure Lengend Snippet: Poly (GR) induces an increase in cyclins and CDKs levels (A) Schematic representation of the CRISPR/Cas9 strategy to generate C9orf72 homozygous and heterozygous lines from a healthy control line. (B) Generation of C9orf72 heterozygous and homozygous knockout iPSC lines by CRISPR Cas9. (C) Representative western blot image of C9orf72 protein levels in homozygous (line 3) and heterozygous (line 8) knockout lines by CRISPR Cas9. (D–G) mRNA levels of Ki67, GMNN, CDK4, and CCNA2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (H) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GR). Scale bars, 200 μm. (I and J) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (K) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GP). Scale bars, 200 μm. (L and M) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (N) Representative western blot image of control iPSC-derived neurons treated with Poly (GR) and poly (GP). (O and P) Quantification of protein levels of CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR) and poly (GP). Data are presented as mean ± SEM (D–G, I and J, L and M, O and P). Data presented in (D–G) is from 3 independent differentiation experiments of a control iPSC line (parental line) and one C9orf72 heterozygous and one homozygous knockout line. Two-tailed t test with Welch’s correction was applied. ns, not significant. Data in (I and J, L and M) is from 3 control iPSC lines treated with DPRs from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. Data in (O and P) is from 3 control iPSC lines treated with DPRs from 2 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Techniques: CRISPR, Control, Knock-Out, Western Blot, Derivative Assay, Immunostaining, Two Tailed Test, Membrane

    CDK4/6 inhibitor Palbociclib (PD33002291) prevents cell-cycle reentry in iPSC-derived motor neuron from C9orf72 carriers (A and B) Western blot and quantification of protein levels of phosphorylated RB and topoisomerase II α (TopoII) in 2-month-old iPSC-derived motor neurons from C9orf72 carriers treated with Palbociclib 1 and 5 μM. (C–E) mRNA levels of Ki67 and CCNA2 and CDK1 in 2-month-old C9orf72 iPSC-derived motor neurons treated with Palbociclib 5 μM. (F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from controls, C9orf72 and C9orf72 neurons treated with Palbociclib 5 μM. (G) Quantification of the percentage of C9orf72 iPSC-derived motor neurons in S-phase. Data are presented as mean ± SEM (A–E, G). Data presented in (A and B) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 treated with Palbociclib 1 and 5 μM from 2 differentiation experiments, one-way ANOVA with Newman-Keuls post hoc test was applied ∗ p < 0.05.∗∗ p < 0.01 and ∗∗∗ p < 0.001. Data presented in (C–E) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 neurons with Palbociclib 5 μM from 2 differentiation experiments. Two-tailed t test with Welch’s correction was applied ∗ p < 0.05 and ∗∗ p < 0.01. Data in (G) is from iPSC-derived neurons from 3 controls, 3 C9orf72 , and 3 C9orf72 treated with Palbociclib from 1 differentiation experiment, one-way ANOVA with Newman-Keuls post hoc test was applied ∗∗ p < 0.01. See also .

    Journal: iScience

    Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD

    doi: 10.1016/j.isci.2025.114596

    Figure Lengend Snippet: CDK4/6 inhibitor Palbociclib (PD33002291) prevents cell-cycle reentry in iPSC-derived motor neuron from C9orf72 carriers (A and B) Western blot and quantification of protein levels of phosphorylated RB and topoisomerase II α (TopoII) in 2-month-old iPSC-derived motor neurons from C9orf72 carriers treated with Palbociclib 1 and 5 μM. (C–E) mRNA levels of Ki67 and CCNA2 and CDK1 in 2-month-old C9orf72 iPSC-derived motor neurons treated with Palbociclib 5 μM. (F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from controls, C9orf72 and C9orf72 neurons treated with Palbociclib 5 μM. (G) Quantification of the percentage of C9orf72 iPSC-derived motor neurons in S-phase. Data are presented as mean ± SEM (A–E, G). Data presented in (A and B) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 treated with Palbociclib 1 and 5 μM from 2 differentiation experiments, one-way ANOVA with Newman-Keuls post hoc test was applied ∗ p < 0.05.∗∗ p < 0.01 and ∗∗∗ p < 0.001. Data presented in (C–E) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 neurons with Palbociclib 5 μM from 2 differentiation experiments. Two-tailed t test with Welch’s correction was applied ∗ p < 0.05 and ∗∗ p < 0.01. Data in (G) is from iPSC-derived neurons from 3 controls, 3 C9orf72 , and 3 C9orf72 treated with Palbociclib from 1 differentiation experiment, one-way ANOVA with Newman-Keuls post hoc test was applied ∗∗ p < 0.01. See also .

    Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

    Techniques: Derivative Assay, Western Blot, Flow Cytometry, Staining, Two Tailed Test

    Expression of CCNA2 in CRC and its effect on biological behavior of CRC cells . A , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by immunohistochemistry assay. B , the mRNA expressions of CCNA2 were detected in paracancerous and CRC tissues by quantitative PCR (qPCR) assay. C , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by Western blotting. D , the protein expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by Western blotting. E , the mRNA expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by qPCR assay. F , the interference efficiency of knockdown CCNA2 expression in the HCT116 and HT29 stable cell lines was evaluated by Western blotting. G , CCK-8 assay showed that knockdown of CCNA2 expression inhibited the proliferation of HT29 and HCT116 cells. H , wound scratch assay demonstrated that hat knockdown of CCNA2 expression inhibited the migration of HT29 and HCT116 cells. I , Transwell assay revealed that knockdown of CCNA2 expression inhibited the invasion of HT29 and HCT116 cells. J , flow cytometry assay indicated that knockdown of CCNA2 expression induced the apoptosis of HT29 and HCT116 cells. K – L , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in HT29 and HCT116 cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Journal: The Journal of Biological Chemistry

    Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

    doi: 10.1016/j.jbc.2025.110216

    Figure Lengend Snippet: Expression of CCNA2 in CRC and its effect on biological behavior of CRC cells . A , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by immunohistochemistry assay. B , the mRNA expressions of CCNA2 were detected in paracancerous and CRC tissues by quantitative PCR (qPCR) assay. C , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by Western blotting. D , the protein expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by Western blotting. E , the mRNA expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by qPCR assay. F , the interference efficiency of knockdown CCNA2 expression in the HCT116 and HT29 stable cell lines was evaluated by Western blotting. G , CCK-8 assay showed that knockdown of CCNA2 expression inhibited the proliferation of HT29 and HCT116 cells. H , wound scratch assay demonstrated that hat knockdown of CCNA2 expression inhibited the migration of HT29 and HCT116 cells. I , Transwell assay revealed that knockdown of CCNA2 expression inhibited the invasion of HT29 and HCT116 cells. J , flow cytometry assay indicated that knockdown of CCNA2 expression induced the apoptosis of HT29 and HCT116 cells. K – L , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in HT29 and HCT116 cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Article Snippet: The slides were treated with primary antibody against CCNA2 (1:500 dilution, #67955; Cell Signaling Technology), primary antibody against ki67 (1:500 dilution, #GB111499-100; ServiceBio) or primary antibody against caspase 3 (1:500 dilution, #GB115600-100; ServiceBio) at 4°C overnight.

    Techniques: Expressing, Immunohistochemistry, Real-time Polymerase Chain Reaction, Western Blot, Knockdown, Stable Transfection, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Assay, Flow Cytometry, Cell Counting

    The miR-548x-3p– CCNA2 axis regulates the biological behavior of CRC cells . A , correlation analysis of miR-548x-3p and CCNA2 mRNA expression in CRC. B , validation of the targeting relationship between miR-548x-3p and CCNA2 through dual-luciferase reporter assays in CRC cells. C , the effect of miR-548x-3p on the targeted regulation of CCNA2 protein expression in CRC cells was analyzed by Western blotting. D , the effect of miR-548x-3p on the targeted regulation of CCNA2 mRNA expression in CRC cells was analyzed by quantitative PCR (qPCR) assay. E , CCK-8 assays demonstrated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the proliferation in CRC cells. F , wound scratch assay indicated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the migration of CRC cells. G , transwell assay showed that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the invasion of CRC cells. H and I , the effect of CCNA2 on miR-548x-3p regulation of the EMT-signaling pathway–associated biomarkers in CRC cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Journal: The Journal of Biological Chemistry

    Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

    doi: 10.1016/j.jbc.2025.110216

    Figure Lengend Snippet: The miR-548x-3p– CCNA2 axis regulates the biological behavior of CRC cells . A , correlation analysis of miR-548x-3p and CCNA2 mRNA expression in CRC. B , validation of the targeting relationship between miR-548x-3p and CCNA2 through dual-luciferase reporter assays in CRC cells. C , the effect of miR-548x-3p on the targeted regulation of CCNA2 protein expression in CRC cells was analyzed by Western blotting. D , the effect of miR-548x-3p on the targeted regulation of CCNA2 mRNA expression in CRC cells was analyzed by quantitative PCR (qPCR) assay. E , CCK-8 assays demonstrated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the proliferation in CRC cells. F , wound scratch assay indicated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the migration of CRC cells. G , transwell assay showed that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the invasion of CRC cells. H and I , the effect of CCNA2 on miR-548x-3p regulation of the EMT-signaling pathway–associated biomarkers in CRC cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Article Snippet: The slides were treated with primary antibody against CCNA2 (1:500 dilution, #67955; Cell Signaling Technology), primary antibody against ki67 (1:500 dilution, #GB111499-100; ServiceBio) or primary antibody against caspase 3 (1:500 dilution, #GB115600-100; ServiceBio) at 4°C overnight.

    Techniques: Expressing, Biomarker Discovery, Luciferase, Western Blot, Real-time Polymerase Chain Reaction, CCK-8 Assay, Over Expression, Wound Healing Assay, Migration, Transwell Assay, Cell Counting

    The effect of CCNA2 on biological behavior of CRC cells in vivo . A , the nude mice with subcutaneous tumorigenesis of shNC and sh CCNA2 CRC cells. B , statistical results of subcutaneous tumor xenograft volume in shNC and sh CCNA2 groups of nude mice. C , the appearance of subcutaneous tumor xenografts in shNC and sh CCNA2 groups of nude mice. D , statistical results of subcutaneous tumor xenograft weight in shNC and sh CCNA2 groups of nude mice. E and F , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in subcutaneous tumor xenografts was analyzed by Western blotting. G , the H&E staining results of subcutaneous tumor xenografts. H and I , the effect of CCNA2 on proliferation and apoptosis-associated biomarkers in subcutaneous tumor xenografts was analyzed by immunohistochemistry. The data in the bar plots were shown as the mean ± SD. ∗ represented p < 0.05; ∗∗ represented p < 0.01; and ∗∗∗ represented p < 0.001. CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Journal: The Journal of Biological Chemistry

    Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

    doi: 10.1016/j.jbc.2025.110216

    Figure Lengend Snippet: The effect of CCNA2 on biological behavior of CRC cells in vivo . A , the nude mice with subcutaneous tumorigenesis of shNC and sh CCNA2 CRC cells. B , statistical results of subcutaneous tumor xenograft volume in shNC and sh CCNA2 groups of nude mice. C , the appearance of subcutaneous tumor xenografts in shNC and sh CCNA2 groups of nude mice. D , statistical results of subcutaneous tumor xenograft weight in shNC and sh CCNA2 groups of nude mice. E and F , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in subcutaneous tumor xenografts was analyzed by Western blotting. G , the H&E staining results of subcutaneous tumor xenografts. H and I , the effect of CCNA2 on proliferation and apoptosis-associated biomarkers in subcutaneous tumor xenografts was analyzed by immunohistochemistry. The data in the bar plots were shown as the mean ± SD. ∗ represented p < 0.05; ∗∗ represented p < 0.01; and ∗∗∗ represented p < 0.001. CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Article Snippet: The slides were treated with primary antibody against CCNA2 (1:500 dilution, #67955; Cell Signaling Technology), primary antibody against ki67 (1:500 dilution, #GB111499-100; ServiceBio) or primary antibody against caspase 3 (1:500 dilution, #GB115600-100; ServiceBio) at 4°C overnight.

    Techniques: In Vivo, Western Blot, Staining, Immunohistochemistry

    Expression of CCNA2 in CRC and its effect on biological behavior of CRC cells . A , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by immunohistochemistry assay. B , the mRNA expressions of CCNA2 were detected in paracancerous and CRC tissues by quantitative PCR (qPCR) assay. C , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by Western blotting. D , the protein expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by Western blotting. E , the mRNA expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by qPCR assay. F , the interference efficiency of knockdown CCNA2 expression in the HCT116 and HT29 stable cell lines was evaluated by Western blotting. G , CCK-8 assay showed that knockdown of CCNA2 expression inhibited the proliferation of HT29 and HCT116 cells. H , wound scratch assay demonstrated that hat knockdown of CCNA2 expression inhibited the migration of HT29 and HCT116 cells. I , Transwell assay revealed that knockdown of CCNA2 expression inhibited the invasion of HT29 and HCT116 cells. J , flow cytometry assay indicated that knockdown of CCNA2 expression induced the apoptosis of HT29 and HCT116 cells. K – L , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in HT29 and HCT116 cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Journal: The Journal of Biological Chemistry

    Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

    doi: 10.1016/j.jbc.2025.110216

    Figure Lengend Snippet: Expression of CCNA2 in CRC and its effect on biological behavior of CRC cells . A , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by immunohistochemistry assay. B , the mRNA expressions of CCNA2 were detected in paracancerous and CRC tissues by quantitative PCR (qPCR) assay. C , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by Western blotting. D , the protein expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by Western blotting. E , the mRNA expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by qPCR assay. F , the interference efficiency of knockdown CCNA2 expression in the HCT116 and HT29 stable cell lines was evaluated by Western blotting. G , CCK-8 assay showed that knockdown of CCNA2 expression inhibited the proliferation of HT29 and HCT116 cells. H , wound scratch assay demonstrated that hat knockdown of CCNA2 expression inhibited the migration of HT29 and HCT116 cells. I , Transwell assay revealed that knockdown of CCNA2 expression inhibited the invasion of HT29 and HCT116 cells. J , flow cytometry assay indicated that knockdown of CCNA2 expression induced the apoptosis of HT29 and HCT116 cells. K – L , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in HT29 and HCT116 cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Article Snippet: The PVDF membranes were blocked with 5% skim milk, and the PVDF membranes were incubated with primary antibodies CCNA2 (1:1000 dilution, #67955; Cell Signaling Technology), E-cadherin (1:1000 dilution, #3195; Cell Signaling Technology), N-cadherin (1:1000 dilution, #13116; Cell Signaling Technology), GAPDH (1:3000 dilution, #AC002; Abclonal), and β-Actin (1:4000 dilution, #90422; SIGMA) at 4°C overnight.

    Techniques: Expressing, Immunohistochemistry, Real-time Polymerase Chain Reaction, Western Blot, Knockdown, Stable Transfection, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Assay, Flow Cytometry, Cell Counting

    The miR-548x-3p– CCNA2 axis regulates the biological behavior of CRC cells . A , correlation analysis of miR-548x-3p and CCNA2 mRNA expression in CRC. B , validation of the targeting relationship between miR-548x-3p and CCNA2 through dual-luciferase reporter assays in CRC cells. C , the effect of miR-548x-3p on the targeted regulation of CCNA2 protein expression in CRC cells was analyzed by Western blotting. D , the effect of miR-548x-3p on the targeted regulation of CCNA2 mRNA expression in CRC cells was analyzed by quantitative PCR (qPCR) assay. E , CCK-8 assays demonstrated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the proliferation in CRC cells. F , wound scratch assay indicated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the migration of CRC cells. G , transwell assay showed that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the invasion of CRC cells. H and I , the effect of CCNA2 on miR-548x-3p regulation of the EMT-signaling pathway–associated biomarkers in CRC cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Journal: The Journal of Biological Chemistry

    Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

    doi: 10.1016/j.jbc.2025.110216

    Figure Lengend Snippet: The miR-548x-3p– CCNA2 axis regulates the biological behavior of CRC cells . A , correlation analysis of miR-548x-3p and CCNA2 mRNA expression in CRC. B , validation of the targeting relationship between miR-548x-3p and CCNA2 through dual-luciferase reporter assays in CRC cells. C , the effect of miR-548x-3p on the targeted regulation of CCNA2 protein expression in CRC cells was analyzed by Western blotting. D , the effect of miR-548x-3p on the targeted regulation of CCNA2 mRNA expression in CRC cells was analyzed by quantitative PCR (qPCR) assay. E , CCK-8 assays demonstrated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the proliferation in CRC cells. F , wound scratch assay indicated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the migration of CRC cells. G , transwell assay showed that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the invasion of CRC cells. H and I , the effect of CCNA2 on miR-548x-3p regulation of the EMT-signaling pathway–associated biomarkers in CRC cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Article Snippet: The PVDF membranes were blocked with 5% skim milk, and the PVDF membranes were incubated with primary antibodies CCNA2 (1:1000 dilution, #67955; Cell Signaling Technology), E-cadherin (1:1000 dilution, #3195; Cell Signaling Technology), N-cadherin (1:1000 dilution, #13116; Cell Signaling Technology), GAPDH (1:3000 dilution, #AC002; Abclonal), and β-Actin (1:4000 dilution, #90422; SIGMA) at 4°C overnight.

    Techniques: Expressing, Biomarker Discovery, Luciferase, Western Blot, Real-time Polymerase Chain Reaction, CCK-8 Assay, Over Expression, Wound Healing Assay, Migration, Transwell Assay, Cell Counting

    The effect of CCNA2 on biological behavior of CRC cells in vivo . A , the nude mice with subcutaneous tumorigenesis of shNC and sh CCNA2 CRC cells. B , statistical results of subcutaneous tumor xenograft volume in shNC and sh CCNA2 groups of nude mice. C , the appearance of subcutaneous tumor xenografts in shNC and sh CCNA2 groups of nude mice. D , statistical results of subcutaneous tumor xenograft weight in shNC and sh CCNA2 groups of nude mice. E and F , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in subcutaneous tumor xenografts was analyzed by Western blotting. G , the H&E staining results of subcutaneous tumor xenografts. H and I , the effect of CCNA2 on proliferation and apoptosis-associated biomarkers in subcutaneous tumor xenografts was analyzed by immunohistochemistry. The data in the bar plots were shown as the mean ± SD. ∗ represented p < 0.05; ∗∗ represented p < 0.01; and ∗∗∗ represented p < 0.001. CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Journal: The Journal of Biological Chemistry

    Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

    doi: 10.1016/j.jbc.2025.110216

    Figure Lengend Snippet: The effect of CCNA2 on biological behavior of CRC cells in vivo . A , the nude mice with subcutaneous tumorigenesis of shNC and sh CCNA2 CRC cells. B , statistical results of subcutaneous tumor xenograft volume in shNC and sh CCNA2 groups of nude mice. C , the appearance of subcutaneous tumor xenografts in shNC and sh CCNA2 groups of nude mice. D , statistical results of subcutaneous tumor xenograft weight in shNC and sh CCNA2 groups of nude mice. E and F , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in subcutaneous tumor xenografts was analyzed by Western blotting. G , the H&E staining results of subcutaneous tumor xenografts. H and I , the effect of CCNA2 on proliferation and apoptosis-associated biomarkers in subcutaneous tumor xenografts was analyzed by immunohistochemistry. The data in the bar plots were shown as the mean ± SD. ∗ represented p < 0.05; ∗∗ represented p < 0.01; and ∗∗∗ represented p < 0.001. CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

    Article Snippet: The PVDF membranes were blocked with 5% skim milk, and the PVDF membranes were incubated with primary antibodies CCNA2 (1:1000 dilution, #67955; Cell Signaling Technology), E-cadherin (1:1000 dilution, #3195; Cell Signaling Technology), N-cadherin (1:1000 dilution, #13116; Cell Signaling Technology), GAPDH (1:3000 dilution, #AC002; Abclonal), and β-Actin (1:4000 dilution, #90422; SIGMA) at 4°C overnight.

    Techniques: In Vivo, Western Blot, Staining, Immunohistochemistry

    A Schematic representation of xenograft tumor of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel, and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. B The weight of xenograft tumor of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel, and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. C The volume of xenograft tumor of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel, and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. D The immunohistochemical staining of IGF2BP3, c-Myc, and Ki-67 of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. Scale bar, 20 μm. E Venn analysis based on c-Myc-targeted genes in GSEA, up-regulated genes in RNA-seq of paclitaxel-resistant Ishikawa cells, and down-regulated genes in RNA-seq of IGF2BP3 knockdown Ishikawa cells. F The immunohistochemical staining of CCNA2 and CCT2 of of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. Scale bar, 20 μm. G Molecular mechanism of IGF2BP3/SPOP/c-Myc loop mediated paclitaxel resistance (Created in BioRender. Zhang, H. (2025) https://BioRender.com/bjcmb9j , Agreement number: DY282PE8YM). Scale bar, 20 μm. Data are shown as mean ± SD ( n ≥ 3). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

    Journal: Communications Biology

    Article Title: The role of IGF2BP3/SPOP/c-Myc loop in paclitaxel resistance of endometrial cancer

    doi: 10.1038/s42003-025-08065-0

    Figure Lengend Snippet: A Schematic representation of xenograft tumor of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel, and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. B The weight of xenograft tumor of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel, and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. C The volume of xenograft tumor of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel, and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. D The immunohistochemical staining of IGF2BP3, c-Myc, and Ki-67 of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. Scale bar, 20 μm. E Venn analysis based on c-Myc-targeted genes in GSEA, up-regulated genes in RNA-seq of paclitaxel-resistant Ishikawa cells, and down-regulated genes in RNA-seq of IGF2BP3 knockdown Ishikawa cells. F The immunohistochemical staining of CCNA2 and CCT2 of of IGF2BP3 overexpression, IGF2BP3 overexpression treated by paclitaxel, IGF2BP3 overexpression plus c-Myc knockdown treated by paclitaxel and IGF2BP3 overexpression treated by paclitaxel and 10058-F4. Scale bar, 20 μm. G Molecular mechanism of IGF2BP3/SPOP/c-Myc loop mediated paclitaxel resistance (Created in BioRender. Zhang, H. (2025) https://BioRender.com/bjcmb9j , Agreement number: DY282PE8YM). Scale bar, 20 μm. Data are shown as mean ± SD ( n ≥ 3). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

    Article Snippet: The following antibodies were used: IGF2BP3 (1:2000 for WB, 1:100 for IHC, Proteintech, 14642-1-AP, Wuhan, China), SPOP (1:5000 for WB, Proteintech, 16750-1-AP, Wuhan, China), c-Myc (1:2000 for WB, 1:50 for IHC, Proteintech, 10828-1-AP, Wuhan, China), GAPDH (Proteintech, 60004-1-Ig, Wuhan, China), Ki-67 (1:500 for IHC, Proteintech, 27309-1-AP, Wuhan, China), CCNA2 (1:50 for IHC, Abclonal, A19036, Wuhan, China), CCT2 (1:50 for IHC, Abclonal, A4700, Wuhan, China), Goat Anti-Rabbit (1:200 for IF, Proteintech, SA00013-4, Wuhan, China), FLAG (1:10000 for WB, MBL, M185-7, Tokyo, Japan), Myc (1:5000 for WB, MBL, M192-7, Tokyo, Japan), HA (1:10000 for WB, MBL, M180-7, Tokyo, Japan), Anti-Rabbit (1:5000 for WB, 1:500 for IHC, Abclonal, AS038, Wuhan, China), anti-mouse (1:50000 for WB, Proteintech, SA00001-1, Wuhan, China).

    Techniques: Over Expression, Knockdown, Immunohistochemical staining, Staining, RNA Sequencing

    Cell cycle regulator proteins expression in different CTR groups. A–H the expression of CCNA2, CCNB1, CCND1, TP53, P16, P21, TOP2A, and pRb in lung adenocarcinoma with different CTR. CTR, consolidation-to-tumour ratio

    Journal: Respiratory Research

    Article Title: Analysis of tumor cell proliferation (Ki-67) and cell cycle regulator proteins in lung adenocarcinoma with different radiological subtypes

    doi: 10.1186/s12931-025-03217-6

    Figure Lengend Snippet: Cell cycle regulator proteins expression in different CTR groups. A–H the expression of CCNA2, CCNB1, CCND1, TP53, P16, P21, TOP2A, and pRb in lung adenocarcinoma with different CTR. CTR, consolidation-to-tumour ratio

    Article Snippet: The antibodies used for the IHC analyses were as follows: CCNB1 (Ab32053, 1:250 dilution; Abcam, MA, USA), P16 (Ab108349, 1:1000 dilution; Abcam, MA, USA), P21 (Ab109520, 1:1000 dilution; Abcam, MA, USA), Cyclin D1 (CCND1) (clone# 5506S, 1:1000 dilution; Cell Signaling Technology, MA, USA), Cyclin A2 (CCNA2) (clone# 67955, 1:1600 dilution; Cell Signaling Technology, MA, USA), TOP2A (12286 T, 1:400 dilution; Cell Signaling Technology, MA, USA), pRb (clone# 8516 T, 1:800 dilution; Cell Signaling Technology, MA, USA), and p53 (Santa Cruz, clone DO1 SC-126, 1:800 dilution; USA).

    Techniques: Expressing

    Differences in the positive expression rate of cell cycle regulatory proteins among different CTR groups. A the TMA constructed using clinical samples (HE staining); B the positive expression rates of GGO-LUAD and SN-LUAD on eight cell cycle regulatory proteins (CCNA2, CCNB1, CCND1, P16, P21, TOP2A, TP53, and pRb). CTR consolidation-to-tumour ratio, TMA tissue microarrays

    Journal: Respiratory Research

    Article Title: Analysis of tumor cell proliferation (Ki-67) and cell cycle regulator proteins in lung adenocarcinoma with different radiological subtypes

    doi: 10.1186/s12931-025-03217-6

    Figure Lengend Snippet: Differences in the positive expression rate of cell cycle regulatory proteins among different CTR groups. A the TMA constructed using clinical samples (HE staining); B the positive expression rates of GGO-LUAD and SN-LUAD on eight cell cycle regulatory proteins (CCNA2, CCNB1, CCND1, P16, P21, TOP2A, TP53, and pRb). CTR consolidation-to-tumour ratio, TMA tissue microarrays

    Article Snippet: The antibodies used for the IHC analyses were as follows: CCNB1 (Ab32053, 1:250 dilution; Abcam, MA, USA), P16 (Ab108349, 1:1000 dilution; Abcam, MA, USA), P21 (Ab109520, 1:1000 dilution; Abcam, MA, USA), Cyclin D1 (CCND1) (clone# 5506S, 1:1000 dilution; Cell Signaling Technology, MA, USA), Cyclin A2 (CCNA2) (clone# 67955, 1:1600 dilution; Cell Signaling Technology, MA, USA), TOP2A (12286 T, 1:400 dilution; Cell Signaling Technology, MA, USA), pRb (clone# 8516 T, 1:800 dilution; Cell Signaling Technology, MA, USA), and p53 (Santa Cruz, clone DO1 SC-126, 1:800 dilution; USA).

    Techniques: Expressing, Construct, Staining

    Associations between Ki-67 and cell cycle regulator proteins expression. A – D the expression of the following four cell cycle regulator proteins showed a positive correlation with Ki-67 expression, namely CCNA2 , TOP2A, TP53, and pRb, E – H the expression of the remaining four cell cycle regulator proteins (included CCNB1, CCND1, P16 and P21) is not correlated with Ki-67 expression

    Journal: Respiratory Research

    Article Title: Analysis of tumor cell proliferation (Ki-67) and cell cycle regulator proteins in lung adenocarcinoma with different radiological subtypes

    doi: 10.1186/s12931-025-03217-6

    Figure Lengend Snippet: Associations between Ki-67 and cell cycle regulator proteins expression. A – D the expression of the following four cell cycle regulator proteins showed a positive correlation with Ki-67 expression, namely CCNA2 , TOP2A, TP53, and pRb, E – H the expression of the remaining four cell cycle regulator proteins (included CCNB1, CCND1, P16 and P21) is not correlated with Ki-67 expression

    Article Snippet: The antibodies used for the IHC analyses were as follows: CCNB1 (Ab32053, 1:250 dilution; Abcam, MA, USA), P16 (Ab108349, 1:1000 dilution; Abcam, MA, USA), P21 (Ab109520, 1:1000 dilution; Abcam, MA, USA), Cyclin D1 (CCND1) (clone# 5506S, 1:1000 dilution; Cell Signaling Technology, MA, USA), Cyclin A2 (CCNA2) (clone# 67955, 1:1600 dilution; Cell Signaling Technology, MA, USA), TOP2A (12286 T, 1:400 dilution; Cell Signaling Technology, MA, USA), pRb (clone# 8516 T, 1:800 dilution; Cell Signaling Technology, MA, USA), and p53 (Santa Cruz, clone DO1 SC-126, 1:800 dilution; USA).

    Techniques: Expressing