ArticleJournal of translational medicine2024
CDCA5 accelerates progression of breast cancer by promoting the binding of E2F1 and FOXM1.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- MND1 reduces breast cancer chemosensitivity by promoting RAD51-mediated homologous recombination repair.Cell death & disease · 2026Article
- Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments.ACS omega · 2026Article
- FOXM1 as a candidate dosage rheostat and state selector in breast cancer: linking multilevel regulation to adaptive plasticity and therapy resistance.Frontiers in oncology · 2026Review
- USP10 stabilizes FOXM1 through KAT5-mediated acetylation to suppress cell senescence and promote melanoma malignant progression.International journal of biological sciences · 2026Article
- High-Throughput Heterospheroid-Based Screening Identifies Drugs That Reprogram Tumor-Associated Macrophages.Journal of immunology research · 2026Article
- The E2F1/SBK1 axis activates the Notch signaling pathway to accelerate the malignant progression of breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- CDCA5 knockdown potentiates olaparib sensitivity in BRCA1-mutated ovarian cancer through autophagy activation.Discover oncology · 2025Article
- Exploring PKMYT1 as a potential marker for colorectal cancer progression through bioinformatics analyses and experimental validation.Scientific reports · 2025Article
- The acidic microenvironment promotes pancreatic cancer progression via the lncRNA-LOC100507424/E2F1/FOXM1 axis.BMC cancer · 2025Article
- E2F1-Dependent CDCA5 overexpression drives cervical cancer progression and correlates with poor prognosis.Journal of molecular histology · 2025Article
- CpG ODN Combined with Gold Nanorods Enhances Immune Activation and Its Potential Mechanism.Journal of inflammation research · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundBreast cancer is one of the most common malignant tumors in women. Cell division cycle associated 5 (CDCA5), a master regulator of sister chromatid cohesion, was reported to be upregulated in several types of cancer. Here, the function and regulation mechanism of CDCA5 in breast cancer were explored.
methodsCDCA5 expression was identified through immunohistochemistry staining in breast cancer specimens. The correlation between CDCA5 expression with clinicopathological features and prognosis of breast cancer patients was analyzed using a tissue microarray. CDCA5 function in breast cancer was explored in CDCA5-overexpressed/knockdown cells and mice models. Co-IP, ChIP and dual-luciferase reporter assay assays were performed to clarify underlying molecular mechanisms.
resultsWe found that CDCA5 was expressed at a higher level in breast cancer tissues and cell lines, and overexpression of CDCA5 was significantly associated with poor prognosis of patients with breast cancer. Moreover, CDCA5 knockdown significantly suppressed the proliferation and migration, while promoted apoptosis in vitro. Mechanistically, we revealed that CDCA5 played an important role in promoting the binding of E2F transcription factor 1 (E2F1) to the forkhead box M1 (FOXM1) promoter. Furthermore, the data of in vitro and in vivo revealed that depletion of FOXM1 alleviated the effect of CDCA5 overexpression on breast cancer. Additionally, we revealed that the Wnt/β-catenin signaling pathway was required for CDCA5 induced progression of breast cancer.
conclusionsWe suggested that CDCA5 promoted progression of breast cancer via CDCA5/FOXM1/Wnt axis, CDCA5 might serve as a novel therapeutic target for breast cancer treatment.
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