ArticleCancer biomarkers : section A of Disease markers2022
E2F1 transcriptionally regulates CCNA2 expression to promote triple negative breast cancer tumorigenicity.
Article in Cancer biomarkers : section A of Disease markers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Acidosis-associated gene signature defines novel subtypes and dual-target therapeutic candidates in breast cancer.Journal of translational medicine · 2026Article
- Metformin Inhibits the Development of Lung Adenocarcinoma by Regulating the Expression of CCNA2Combinatorial chemistry & high throughput screening · 2026Article
- Unveiling immune-related gene signatures in triple negative breast cancer through integrated transcriptomic analysis.BioMedicine · 2026Article
- Noncanonical association of EZH2 with E2F1 promotes tumor proliferation through chromatin remodeling.Experimental & molecular medicine · 2025Article
- PSMD14/E2F1 Axis-Mediated CENPF Promotes the Metastasis of Triple-Negative Breast Cancer Through Inhibiting Ferroptosis.Cancer science · 2025Article
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- Investigating the molecular mechanisms, drug prediction, and validation of CCNA2 and MAD2L1 in esophageal squamous cell carcinoma based on bioinformatics.BMC medical genomics · 2025Article
- Differential roles of cyclin-CDK1 complexes in cell migration and invasion.Journal of cell science · 2025Article
- Berberine diminishes the malignant progression of non-small cell lung cancer cells by targeting CDCA5 and CCNA2.Journal of natural medicines · 2025Article
- Gene Expression Signatures of Porcine Bone Marrow-Derived Antigen-Presenting Cells Infected with Classical Swine Fever Virus.Viruses · 2025Article
- Comprehensive analysis pinpoints CCNA2 as a prognostic and immunological biomarker in non-small cell lung cancer.BMC pulmonary medicine · 2025Article
- Transcriptomic Analysis of HPV-Positive Oesophageal Tissue Reveals Upregulation of Genes Linked to Cell Cycle and DNA Replication.International journal of molecular sciences · 2024Article
- Integrated analysis of hub genes and intrinsically disordered regions in triple-negative breast cancer.Journal, genetic engineering & biotechnology · 2024Article
- Clinical significance of upregulated Rho GTPase activating protein 12 causing resistance to tyrosine kinase inhibitors in hepatocellular carcinoma.World journal of gastrointestinal oncology · 2024Article
- Deciphering the miRNA-mRNA Interaction Landscape between Breast Cancer and Triple-Negative Breast Cancer: An Integrated Bioinformatics Approach.ACS omega · 2024Article
- SETD7 Promotes Cell Proliferation and Migration via Methylation-mediated TAF7 in Clear Cell Renal Cell Carcinoma.International journal of biological sciences · 2024Article
- Tanshinone IIA Inhibits Triple-Negative Breast Cancer Cells MDA-MB-231 via G Protein-Coupled Estrogen Receptor- (GPER-) Dependent Signaling Pathway.Disease markers · 2023Article
- Analysis of two-gene signatures and related drugs in small-cell lung cancer by bioinformatics.Open medicine (Warsaw, Poland) · 2023Article
- Integrating single-cell RNA-seq and bulk RNA-seq to construct prognostic signatures to explore the role of glutamine metabolism in breast cancer.Frontiers in endocrinology · 2023Article
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Authors and funding
9 authors.
Funding
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Abstract
backgroundTriple-negative breast cancer (TNBC) is a highly malignant breast cancer subtype with a poor prognosis. The cell cycle regulator cyclin A2 (CCNA2) plays a role in tumor development. Herein, we explored the role of CCNA2 in TNBC.
methodsWe analyzed CCNA2 expression in 15 pairs of TNBC and adjacent tissues and assessed the relationship between CCNA2 expression using the tissue microarray cohort. Furthermore, we used two TNBC cohort datasets to analyze the correlation between CCNA2 and E2F transcription factor 1 (E2F1) and a luciferase reporter to explore their association. Through rescue experiments, we analyzed the effects of E2F1 knockdown on CCNA2 expression and cellular behavior.
resultsWe found that CCNA2 expression in TNBC was significantly higher than that in adjacent tissues with similar observations in MDA-MB-231 and MDA-MB-468 cells. E2F1 was highly correlated with CCNA2 as observed through bioinformatics analysis (R= 0.80, P< 0.001) and through TNBC tissue verification analysis (R= 0.53, P< 0.001). We determined that E2F1 binds the +677 position within the CCNA2 promoter. Moreover, CCNA2 overexpression increased cell proliferation, invasion, and migration owing to E2F1 upregulation in TNBC.
conclusionOur data indicate that E2F1 promotes TNBC proliferation and invasion by upregulating CCNA2 expression. E2F1 and CCNA2 are potential candidates that may be targeted for effective TNBC treatment.
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