Review




Structured Review

Proteintech cyclin e1
A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, <t>Cyclin</t> <t>E1,</t> CDK2, p-CDK2); combination treatment increased p27 and decreased <t>Cyclin</t> <t>E1,</t> CDK2, and p-CDK2 (representative of three independent experiments).
Cyclin E1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 51 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "Dual targeting of PI3Kδ and PPARα enhances antitumor activity via FoxO1 activation in follicular lymphoma"

Article Title: Dual targeting of PI3Kδ and PPARα enhances antitumor activity via FoxO1 activation in follicular lymphoma

Journal: Cell Death & Disease

doi: 10.1038/s41419-026-08593-5

A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, Cyclin E1, CDK2, p-CDK2); combination treatment increased p27 and decreased Cyclin E1, CDK2, and p-CDK2 (representative of three independent experiments).
Figure Legend Snippet: A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, Cyclin E1, CDK2, p-CDK2); combination treatment increased p27 and decreased Cyclin E1, CDK2, and p-CDK2 (representative of three independent experiments).

Techniques Used: DNA Synthesis, Staining, Western Blot



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A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, <t>Cyclin</t> <t>E1,</t> CDK2, p-CDK2); combination treatment increased p27 and decreased <t>Cyclin</t> <t>E1,</t> CDK2, and p-CDK2 (representative of three independent experiments).
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Image Search Results


A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, Cyclin E1, CDK2, p-CDK2); combination treatment increased p27 and decreased Cyclin E1, CDK2, and p-CDK2 (representative of three independent experiments).

Journal: Cell Death & Disease

Article Title: Dual targeting of PI3Kδ and PPARα enhances antitumor activity via FoxO1 activation in follicular lymphoma

doi: 10.1038/s41419-026-08593-5

Figure Lengend Snippet: A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, Cyclin E1, CDK2, p-CDK2); combination treatment increased p27 and decreased Cyclin E1, CDK2, and p-CDK2 (representative of three independent experiments).

Article Snippet: The primary antibodies used were as follows: PI3K p110δ (A19742; ABclonal), pan-Akt (#4691; CST), phospho-Akt (Ser473, #4060; CST), PPARα (ab227074; Abcam), FoxO1 (#2880; CST), phospho-FoxO1 (Thr24, #9464; CST) and (Ser256, #9461; CST), FoxO3a (#12829; CST), FoxO4 (#9472; CST), Mcl-1 (#16225-1-AP; Proteintech), Bcl-2 (#12789-1-AP; Proteintech), Bim (A19702; ABclonal), Bax (#50599-2-Ig; Proteintech), Cleaved PARP(#5625; CST), P21(#2947; CST), p27 (#3686; CST), Cyclin E1 (#11935-1-AP; Proteintech), CDK2 (#10122-1-AP; Proteintech), phospho-CDK2 (#4539; CST), GLUT1(#73015; CST), PGK1(A12686; ABclonal), β-Tubulin (#10094-1-AP; Proteintech), Lamin B1 (#13435; CST), and β-Actin (#66009-1-Ig; Proteintech).

Techniques: DNA Synthesis, Staining, Western Blot

Identification and biomarkers (A–C) PPI network: The interaction of 23 candidate genes (A), CCNE1 (B), and UGT1A6 (C). (D–F) The top 15 genes acquired by Radiality (D), Closeness (E), and Degree algorithms (F). (G) Venn diagram of intersecting genes from the above 3 algorithms with the module genes. (H–I) Box plot analysis indicated the hub genes in the training set and validation set.

Journal: ACS Omega

Article Title: Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments

doi: 10.1021/acsomega.5c11680

Figure Lengend Snippet: Identification and biomarkers (A–C) PPI network: The interaction of 23 candidate genes (A), CCNE1 (B), and UGT1A6 (C). (D–F) The top 15 genes acquired by Radiality (D), Closeness (E), and Degree algorithms (F). (G) Venn diagram of intersecting genes from the above 3 algorithms with the module genes. (H–I) Box plot analysis indicated the hub genes in the training set and validation set.

Article Snippet: Primary antibodies against Cyclin E1 (HUABIO, ET1612–16; 1:2000), EZH2 (HUABIO, HA722095; 1:2000), E2F1 (HUABIO, ET1701–73; 1:2000), CDK1 (Affinity, DF6024; 1:2000), E-cadherin (Abcam, ab314063; 1:1000), vimentin (Abcam, ab8978; 1:2000), MMP2 (Abcam, ab92536; 1:2000), MMP9 (HUABIO, ET1704–69; 1:4000), and GADPH (HUABIO, HA721136; 1:20,000) were used.

Techniques: Biomarker Discovery

Pathways enriched with biomarkers in BRCA (A–D) GSEA revealed the enriched pathway of (A) CDK1, (B) E2F1, (C) EZH2, and (D) CCNE1.

Journal: ACS Omega

Article Title: Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments

doi: 10.1021/acsomega.5c11680

Figure Lengend Snippet: Pathways enriched with biomarkers in BRCA (A–D) GSEA revealed the enriched pathway of (A) CDK1, (B) E2F1, (C) EZH2, and (D) CCNE1.

Article Snippet: Primary antibodies against Cyclin E1 (HUABIO, ET1612–16; 1:2000), EZH2 (HUABIO, HA722095; 1:2000), E2F1 (HUABIO, ET1701–73; 1:2000), CDK1 (Affinity, DF6024; 1:2000), E-cadherin (Abcam, ab314063; 1:1000), vimentin (Abcam, ab8978; 1:2000), MMP2 (Abcam, ab92536; 1:2000), MMP9 (HUABIO, ET1704–69; 1:4000), and GADPH (HUABIO, HA721136; 1:20,000) were used.

Techniques:

The binding ability of MEP to biomarkers Molecular docking models of (A) CDK1, (B) E2F1, (C) EZH2, and (D) CCNE1 with MEP. (E) RMSD analysis of protein backbone atoms during 100 ns MD simulations. (F) RMSF analysis of protein backbone atoms during 100 ns MD simulations. (G) Rg analysis of protein backbone atoms during 100 ns simulations.

Journal: ACS Omega

Article Title: Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments

doi: 10.1021/acsomega.5c11680

Figure Lengend Snippet: The binding ability of MEP to biomarkers Molecular docking models of (A) CDK1, (B) E2F1, (C) EZH2, and (D) CCNE1 with MEP. (E) RMSD analysis of protein backbone atoms during 100 ns MD simulations. (F) RMSF analysis of protein backbone atoms during 100 ns MD simulations. (G) Rg analysis of protein backbone atoms during 100 ns simulations.

Article Snippet: Primary antibodies against Cyclin E1 (HUABIO, ET1612–16; 1:2000), EZH2 (HUABIO, HA722095; 1:2000), E2F1 (HUABIO, ET1701–73; 1:2000), CDK1 (Affinity, DF6024; 1:2000), E-cadherin (Abcam, ab314063; 1:1000), vimentin (Abcam, ab8978; 1:2000), MMP2 (Abcam, ab92536; 1:2000), MMP9 (HUABIO, ET1704–69; 1:4000), and GADPH (HUABIO, HA721136; 1:20,000) were used.

Techniques: Binding Assay

Key cells in the scRNA-seq data (A, B) Relative comparison of spatial clusters between the BRCA and the control samples. (C–F) The violin plot revealed the expression level of (C) CDK1, (D) E2F1, (E) EZH2, and (F) CCNE1 in different cell subsets between the BRCA samples versus. controls. (G) KEGG results for fibroblasts between the BRCA samples versus. controls.

Journal: ACS Omega

Article Title: Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments

doi: 10.1021/acsomega.5c11680

Figure Lengend Snippet: Key cells in the scRNA-seq data (A, B) Relative comparison of spatial clusters between the BRCA and the control samples. (C–F) The violin plot revealed the expression level of (C) CDK1, (D) E2F1, (E) EZH2, and (F) CCNE1 in different cell subsets between the BRCA samples versus. controls. (G) KEGG results for fibroblasts between the BRCA samples versus. controls.

Article Snippet: Primary antibodies against Cyclin E1 (HUABIO, ET1612–16; 1:2000), EZH2 (HUABIO, HA722095; 1:2000), E2F1 (HUABIO, ET1701–73; 1:2000), CDK1 (Affinity, DF6024; 1:2000), E-cadherin (Abcam, ab314063; 1:1000), vimentin (Abcam, ab8978; 1:2000), MMP2 (Abcam, ab92536; 1:2000), MMP9 (HUABIO, ET1704–69; 1:4000), and GADPH (HUABIO, HA721136; 1:20,000) were used.

Techniques: Comparison, Control, Expressing

MEP promote the malignant biological behavior of MCF-7 (A) qRT-PCR data showing CDK1, EZH2, E2F1, and CCNE1 mRNA expression. (B) Western blots showing CDK1, EZH2, E2F1, and CCNE1 expression. (C) Macrographs of colony formation and quantitative analysis. (D) Flow cytometry showing cell cycle distribution and cell percentages in different phases. (E) Wound healing assay with quantitative analysis was performed to assess the migratory capacity. Scale bar 650 μm. (F) Representative cell migration images and migration index. Scale bar 275 μm. (G) Phalloidin staining was employed to evaluate F-actin reorganization. Scale bar 25 μm. (H) Western blots showing E-cadherin, Vimentin, MMP2, and MMP9 expression. Data are presented as the mean ± standard deviation ( n = 3), * P < 0.05, ** P < 0.01, *** P < 0.001 and **** P < 0.0001 when compared with control cells.

Journal: ACS Omega

Article Title: Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments

doi: 10.1021/acsomega.5c11680

Figure Lengend Snippet: MEP promote the malignant biological behavior of MCF-7 (A) qRT-PCR data showing CDK1, EZH2, E2F1, and CCNE1 mRNA expression. (B) Western blots showing CDK1, EZH2, E2F1, and CCNE1 expression. (C) Macrographs of colony formation and quantitative analysis. (D) Flow cytometry showing cell cycle distribution and cell percentages in different phases. (E) Wound healing assay with quantitative analysis was performed to assess the migratory capacity. Scale bar 650 μm. (F) Representative cell migration images and migration index. Scale bar 275 μm. (G) Phalloidin staining was employed to evaluate F-actin reorganization. Scale bar 25 μm. (H) Western blots showing E-cadherin, Vimentin, MMP2, and MMP9 expression. Data are presented as the mean ± standard deviation ( n = 3), * P < 0.05, ** P < 0.01, *** P < 0.001 and **** P < 0.0001 when compared with control cells.

Article Snippet: Primary antibodies against Cyclin E1 (HUABIO, ET1612–16; 1:2000), EZH2 (HUABIO, HA722095; 1:2000), E2F1 (HUABIO, ET1701–73; 1:2000), CDK1 (Affinity, DF6024; 1:2000), E-cadherin (Abcam, ab314063; 1:1000), vimentin (Abcam, ab8978; 1:2000), MMP2 (Abcam, ab92536; 1:2000), MMP9 (HUABIO, ET1704–69; 1:4000), and GADPH (HUABIO, HA721136; 1:20,000) were used.

Techniques: Quantitative RT-PCR, Expressing, Western Blot, Flow Cytometry, Wound Healing Assay, Migration, Staining, Standard Deviation, Control

(A) Representative Western blot, (B) densitometry analysis, and (C) qRT-PCRs showing that there were no significant effects of mutEpCAM on protein expression for any of the tested downstream targets of EpCAM including the epidermal growth factor receptor ( EGFR ), E-cadherin ( CDH1 ), β-catenin ( CTNNB1 ), cyclin E ( CCNE ), cyclin A ( CCNA ), and c-myc ( MYC ). N = 3 for all groups and targets for A-B and N = 4 for all groups and targets for C . All comparisons were performed on GraphPad Prism using a two-way ANOVA with Dunnett’s multiple comparisons test (* denotes p < 0.05, **denotes p < 0.01, ***denotes p < 0.001). Uncropped, full-length Western blots are shown in Supplementary Fig. .

Journal: Scientific Reports

Article Title: Functional effects of EpCAM N-glycosylation in MDA-MB-468 breast cancer cells

doi: 10.1038/s41598-026-38920-x

Figure Lengend Snippet: (A) Representative Western blot, (B) densitometry analysis, and (C) qRT-PCRs showing that there were no significant effects of mutEpCAM on protein expression for any of the tested downstream targets of EpCAM including the epidermal growth factor receptor ( EGFR ), E-cadherin ( CDH1 ), β-catenin ( CTNNB1 ), cyclin E ( CCNE ), cyclin A ( CCNA ), and c-myc ( MYC ). N = 3 for all groups and targets for A-B and N = 4 for all groups and targets for C . All comparisons were performed on GraphPad Prism using a two-way ANOVA with Dunnett’s multiple comparisons test (* denotes p < 0.05, **denotes p < 0.01, ***denotes p < 0.001). Uncropped, full-length Western blots are shown in Supplementary Fig. .

Article Snippet: Antibodies used were anti-EpCAM antibody (1:500 dilution; Santa Cruz Biotechnology #sc25308); anti-α-tubulin antibody (1:500 dilution, Sigma Aldrich #T5168); anti-Ku70 antibody (1:500 dilution, Cell Signaling Technology #4588S, Danvers, MA, USA); anti-EGFR antibody (1:2,000 dilution, Proteintech #66455-1-Ig, Rosemont, IL, USA); anti-E-cadherin antibody (1:1,000 dilution, Proteintech #20874-1-AP); anti-β-catenin antibody (1:250 dilution, Cell Signaling Technology #8814S); anti-cyclin E antibody (1:100 dilution, Cell Signaling Technology #4129S); anti-cyclin A antibody (1:500 dilution, Santa Cruz Biotechnology #sc271882); anti-GAPDH antibody (1:3,000 dilution, Sigma Aldrich #G8795); anti-mouse IgG, HRP-linked antibody (1:2,000 dilution, Cell Signaling Technology #7076S); anti-rabbit IgG, HRP-linked antibody (1:2,000 dilution, Cell Signaling Technology #7074S).

Techniques: Western Blot, Expressing