CENPF facilitates endometrial cancer cell progression through PI3K/AKT/mTOR pathway

Centromere protein F (CENPF) has been found to exert vital roles in various cancers, while the detailed effect of CENPF on endometrial cancer (EC) remains unclear. This study indicated that CENPF was up-regulated in EC tissue samples using The University of ALabama at Birmingham CANcer data analysis Portal (UALCAN) and Gene Expression Profiling Interactive Analysis (GEPIA) database. Quantitative real time polymerase chain reaction and western blotting assays confirmed the increased CENPF in EC cells. In addition, overexpression of CENPF promoted cell proliferation, whereas CENPF knockdown notably suppressed the proliferation of EC cells, demonstrated by Methyl Thiazolyl Tetrazolium (MTT) as well as colony formation assays. Moreover, CENPF overexpression accelerated cell cycle, migration ad invasion, whereas CENPF knockdown contributed to cell cycle arrest at G2 stage and suppressed migration and invasion in EC cells. Furthermore, western blotting analysis demonstrated that CENPF overexpression up-regulated the content of phosphorylated protein kinase B (p-AKT), phosphorylated phosphatidylinositol 3-kinase (p-PI3K), and phosphorylated mechanistic target of rapamycin kinase (p-mTOR), while CENPF silencing notably decreased their levels, indicating that CENPF positively regulated PI3K/AKT/mTOR signaling in EC cells. In summary, this study verified that CENPF promoted EC cells progression by mediating PI3K/AKT/mTOR cascade signal in EC cell lines.

Endometrial cancer; CENPF; Proliferation; Cell cycle; PI3K/AKT/mTOR signaling pathway

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