ArticleOncology letters2021
Knockdown of NCOA5 suppresses viability, migration and epithelial-mesenchymal transition, and induces adhesion of breast cancer cells.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Prmt1-mediated histone H4R3me2a methylation regulates the proliferation, migration and invasion of laryngeal cancer cells by affecting the expression level of NCOA5.Frontiers in oncology · 2024Article
- Role of the TPX2/NCOA5 axis in regulating proliferation, migration, invasion and angiogenesis of breast cancer cells.Experimental and therapeutic medicine · 2023Article
- Expression and clinical significance of NCOA5 in epithelial ovarian cancer.Frontiers in oncology · 2023Article
- Data mining identifies novel RNA-binding proteins involved in colon and rectal carcinomas.Frontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear receptor coactivator 5 (NCOA5) has been reported to be involved in the regulation of several malignancies; however, to the best of our knowledge, its role in breast cancer is still unknown. The present study aimed to reveal the biological function of NCOA5 in breast cancer cells. NCOA5 expression in breast cancer tissues and cell lines was examined using reverse transcription-quantitative PCR and western blotting. Small interfering RNA (siRNA) against NCOA5 (siNCOA5) was transfected into MDA-MB-453 and MCF-7 cells to knock down NCOA5. MTT, transwell migration and cell adhesion assays were performed to determine cell viability, migration and adhesion abilities of breast cancer cells, respectively. In addition, the expression levels of N-cadherin, Vimentin and E-cadherin were examined by western blotting. It was revealed that NCOA5 expression was significantly increased in breast cancer tissues and cell lines. Knockdown of NCOA5 suppressed breast cancer cell viability and migration, and induced cell adhesion. Compared with those in cells transfected with non-targeting negative control siRNA, the protein expression levels of N-cadherin and Vimentin were significantly decreased, whereas the protein expression levels of E-cadherin were significantly increased in cells transfected with siNCOA5. The present study demonstrated that knockdown of NCOA5 suppressed cell viability and migration, induced cell adhesion, and inhibited epithelial-mesenchymal transition of breast cancer cells, indicating that NCOA5 may serve a tumor-promoting role in breast cancer.
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Registered trials
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