Knockdown of E2F4 suppresses the growth of ovarian cancer cells through the cell cycle pathway

xlomafota13 shared this article with you from Inoreader Knockdown of E2F4 suppresses the growth of ovarian cancer cells through the cell cycle pathway Via International Journal of Clinical and Experimental Pathology Int J Clin Exp Pathol. 2021 Aug 15;14(8):866-874. eCollection 2021. ABSTRACT Ovarian cancer remains one of the major causes of death from gynecologic cancer in developed countries. The E2F family has been shown to have a central role in the control of cell proliferation, differentiation, and cell cycle progression in various types of cancer. Despite advances in cancer research, the carcinogenic role of E2F transcription factor 4 (E2F4) in ovarian cancer remains unclear. In this study, we investigated the underlying molecular mechanism of E2F4 in human ovarian cancer cells (OCC). E2F4 expression was demonstrated by quantitative real time polymerase chain reaction (qRT-PCR) in OCC. The alterations of expression values were determined using 2(-ΔΔCt) method. The effects of suppressing E2F4 on cell proliferation, migration, and differentiation were evaluated by cell proliferation assay, colony formation assay and wound healing assay in vitro. Overexpression of E2F4 was found at both mRNA and protein levels in OCC. Small interfering RNA was used to suppress E2F4 expression. Depletion of E2F4 inhibited cell proliferation and suppressed the cell migration and colony formation ability compared to controls. The expression of cell cycle machinery including cyclin A, cyclin D and cyclin dependent kinase 2 (CDK2) was increased after E2F4 knockdown. E2F4 modulates ovarian cancer cell proliferation and migration through cell cycle components including cyclin A, cyclin D, and CDK2. Our findings indicate that E2F4 may serve as a valuable candidate and therapeutic target for ovarian cancer treatment in regard to cell cycle control. PMID:34527129 | PMC:PMC8414426 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.