Journal: The FASEB Journal

Article Title: G9a promotes cell proliferation and suppresses autophagy in gastric cancer by directly activating mTOR

doi: 10.1096/fj.201900233rr

Figure Lengend Snippet: Figure 2. Down-regulation of G9a represses cell proliferation of GC. A) Western blotting and real-time qPCR assays were performed to detect the G9a expression in 3 G9a-knockdown GC cell lines. Tubulin was used as a loading control. B) G9a knockdown repressed the growth and proliferation of HGC-27, MKN-45, and SGC-7901 cells. Cell viability was detected using CCK8 assays. C) GC cells were treated with BIX01294 and analyzed for cell viability using CCK8 assays. D) Ki67 immunofluorescence assays were performed after G9a knockdown or inhibition. Cells were treated with 7 mM BIX01294 for 48 h. Representative images show immunofluorescence. Scale bars, 20 mm. All data are shown as means 6 SD; n = 3. *P , 0.05, **P , 0.01, ***P , 0.001.

Article Snippet: G9a (ab40542), Ki67 (ab92742), Unc-51–like autophagyactivating kinase 1 (ULK1; ab128859), Beclin-1 (ab207612), p62/ SQSTM1 (ab207305), mTOR (ab32028), H3K9me1 (ab9045), H3K9me2 (ab1220), and p-H3S10 (5176) antibodies were purchased from Abcam (Cambridge, MA, USA). p(Ser2448)-mTOR (D9C2), CyclinA2 (BF683), CyclinB1 (D5C10), p(Ser757)-ULK1 (D7O6U), p70S6K (D5U1O), CDK1 (POH1), and LC3B (D11) were purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Western Blot, Expressing, Knockdown, Control, Inhibition

Journal: The FASEB Journal

Article Title: G9a promotes cell proliferation and suppresses autophagy in gastric cancer by directly activating mTOR

doi: 10.1096/fj.201900233rr

Figure Lengend Snippet: Figure 3. Down-regulation of G9a represses colony formation in vitro and tumor formation of GC cells in vivo. A, B) The effects of G9a on the colony formation in 3 G9a-knockdown GC cell lines. Scale bars, 20 mm. The colony numbers in plate were quantified. C, D) The tumor growth curve and tumor weight of G9a knockdown GC cells injected into NOD-SCID mice. E) Immunohistochemical (IHC) staining of G9a expression (left) and Ki67 expression (right). Scale bars, 20 mm. F) The quantification of G9a-positive cells (left) and Ki67-positive cells (right). All data are shown as means 6 SD; n = 3. **P , 0.01, ***P , 0.001.

Article Snippet: G9a (ab40542), Ki67 (ab92742), Unc-51–like autophagyactivating kinase 1 (ULK1; ab128859), Beclin-1 (ab207612), p62/ SQSTM1 (ab207305), mTOR (ab32028), H3K9me1 (ab9045), H3K9me2 (ab1220), and p-H3S10 (5176) antibodies were purchased from Abcam (Cambridge, MA, USA). p(Ser2448)-mTOR (D9C2), CyclinA2 (BF683), CyclinB1 (D5C10), p(Ser757)-ULK1 (D7O6U), p70S6K (D5U1O), CDK1 (POH1), and LC3B (D11) were purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: In Vitro, In Vivo, Knockdown, Injection, Immunohistochemical staining, Immunohistochemistry, Expressing

Journal: Cancer Research Communications

Article Title: Novel Syngeneic Cell Lines for Studying High-Risk BRAF V600E -Driven Colorectal Cancer In Vivo

doi: 10.1158/2767-9764.CRC-25-0599

Figure Lengend Snippet: All NaJa cell lines successfully engraft into syngeneic immunocompetent C57BL/6N mice and recapitulate their individual 2D morphologies in vivo . A, Schematic overview of the PVI of NaJa cells ( n = 2 NaJa-D, n = 10 NaJa-F, and n = 3 NaJa-G). B, Left, livers showing metastatic nodules 4 weeks after injection (black arrows) and invasive growth in the pancreatic tissue (blue circles). Scale bar, 1 cm. Hematoxylin and eosin: Histology showing that all NaJa cell lines establish tumors (pale blue) in the liver parenchyma (pink) with a differentiation state matching their epithelial or mesenchymal in vitro morphology. Right, IHC and immunofluorescence (IF) staining of proliferation marker Ki-67 (left) and intestinal differentiation markers CDX2 (middle) and E-cadherin (right). L, liver; T, tumor. Scale bar (overview), 500 μm, scale bar (zoom, IHC, and IF), 50 μm. C, Quantification of Ki-67 and CDX2 IHC staining in NaJa cell–induced liver metastases. Each dot represents an individual tumor; different shapes indicate individual tissue sections, and colors denote individual mice. Data are shown as the median ±95% confidence interval (CI).Statistical significance was assessed using the Kruskal–Wallis test followed by Dunn multiple comparison test. **, P < 0.01; ****, P < 0.0001. D, IHC staining of ERK and its downstream target DUSP6. Red arrows indicate examples of nuclear ERK staining. L, liver; T, tumor. Scale bar, 50 μm. [ A, Created by J. Traichel in BioRender. Brummer, T. (2025) https://BioRender.com/8ogg64c .]

Article Snippet: The formalin-fixed, paraffin-embedded (FFPE) sections underwent standard processing and staining procedures using the following primary antibodies directed against E-cadherin (1:50, #610181, BD Laboratories; RRID: AB_397580) and Ki-67 (1:400, #9129, Cell Signaling Technology; RRID: AB_2687446).

Techniques: In Vivo, Injection, In Vitro, Immunofluorescence, Staining, Marker, Immunohistochemistry, Comparison

Journal: Frontiers in Endocrinology

Article Title: Ultrasound combined with microbubbles promotes diabetic wound healing by regulating macrophage polarization

doi: 10.3389/fendo.2026.1781906

Figure Lengend Snippet: Immunohistochemical staining of wounds in diabetic rats. (A) Representative images of Ki67 immunohistochemical staining in healing tissues from three experimental groups; (B) Quantitative analysis of Ki67-positive cells across groups; (C) Immunohistochemical staining of CD31 in diabetic wounds; (D) Statistical results of CD31-positive expression. Data are presented as mean ± SD (n = 4); *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: After three washes with PBS, they were incubated overnight at 4 °C with anti-CD31 antibodies (1:1000, abcam) and anti-Ki67 antibodies (1:1000, Proteintech).

Techniques: Immunohistochemical staining, Staining, Expressing

Journal: The veterinary quarterly

Article Title: Multiple roles of LncRNA-BMNCR on cell proliferation and apoptosis by targeting miR-145/CBFB axis in BMECs.

doi: 10.1080/01652176.2023.2262525

Figure Lengend Snippet: Figure 2. BMNCR Facilitated proliferation and attenuated apoptosis in BMECs. (A) qRT-PCR detected the expression efficiency of BMNCR after transfected three BMNCR siRNAs, respectively. (B) The expression levels of inflammation-related cytokines were validated by RT‐qPCR after treated siBMNCR for 48 h. (C) CCK8 assay exploring the function of BMNCR on the viability of BMECs. (D) EdU assay detected the number of BMECs treated with siBMNCR. (E) The proportion of EdU positive cells was counted by ImageJ. (F) Cell apoptosis was determined by flow cytometry after transfected with siBMNCR. (G) Distribution map of BMECs apoptosis. (H) Cell apoptosis index was counted by the sum of early and late apoptosis. Data are means ± SE of n = 3 independent experiments, each performed in triplicate, and normalized to GAPDH. *, p < .05 and **, p < .01.

Article Snippet: Finally, cells were stained using the Cell Proliferation Assay Kit (C0075S, Beyotime, Shanghai, China), and images were collected on the Inverted Fluorescence Microscope (DMi8, Leica, Germany).

Techniques: Quantitative RT-PCR, Expressing, Transfection, CCK-8 Assay, EdU Assay, Flow Cytometry

Journal: The veterinary quarterly

Article Title: Multiple roles of LncRNA-BMNCR on cell proliferation and apoptosis by targeting miR-145/CBFB axis in BMECs.

doi: 10.1080/01652176.2023.2262525

Figure Lengend Snippet: Figure 4. Functional roles of miR-145 on proliferation and apoptosis of BMECs. (A) qRT-PCR detected the overexpression (mimic) or Interference (inhibitor) efficiency of miR-145. The expression levels of inflammation-related cytokines were validated by RT‐qPCR after treated miR-145 mimic (B) or miR-145 inhibitor (C). (D) EdU assay detected the number of BMECs after treated with miR-145 mimic or inhibitor. (E) The proportion of EdU positive cells was counted by ImageJ. (F) Cell apoptosis was determined by flow cytometry after transfected with miR-145 mimic or inhibitor. (G) Distribution map of BMECs apoptosis. (H) Cell apoptosis index was counted by the sum of early and late apoptosis. Data are means ± SE of n = 3 independent exper iments, each performed in triplicate, and normalized to GAPDH. *, p < .05 and **, p < .01.

Article Snippet: Finally, cells were stained using the Cell Proliferation Assay Kit (C0075S, Beyotime, Shanghai, China), and images were collected on the Inverted Fluorescence Microscope (DMi8, Leica, Germany).

Techniques: Functional Assay, Quantitative RT-PCR, Over Expression, Expressing, EdU Assay, Flow Cytometry, Transfection

Journal: The veterinary quarterly

Article Title: Multiple roles of LncRNA-BMNCR on cell proliferation and apoptosis by targeting miR-145/CBFB axis in BMECs.

doi: 10.1080/01652176.2023.2262525

Figure Lengend Snippet: Figure 7. CBFB could modulate proliferation and apoptosis in BMECs. (A) qRT-PCR detected the expression efficiency of CBFB after transfected three siRNAs of CBFB, respectively. After transfected siCBFB into BMECs for 48 h, (B) mRNA level of CBFB was explored by qRT-PCR. (C) The protein level of CBFB was explored by Western blot. (D) The relative protein level of CBFB was calculated by ImageJ. (E) The expression levels of inflammation-related cytokines were validated by RT‐qPCR after treated siCBFB into BMECs for 48h. (F) EdU assay detected the number of BMECs treated with siCBFB. (G) The proportion of EdU positive cells was counted by ImageJ. (H) Cell apoptosis was determined by flow cytometry after transfected with siCBFB. (I) Distribution map of BMECs apoptosis. (J) Cell apoptosis index was counted by the sum of early and late apoptosis. Data are means ± SE of n = 3 independent experiments, each performed in triplicate, and normalized to GAPDH. *, p < .05 and **, p < .01.

Article Snippet: Finally, cells were stained using the Cell Proliferation Assay Kit (C0075S, Beyotime, Shanghai, China), and images were collected on the Inverted Fluorescence Microscope (DMi8, Leica, Germany).

Techniques: Quantitative RT-PCR, Expressing, Transfection, Western Blot, EdU Assay, Flow Cytometry