Inhibition of TMEM45A suppresses proliferation, induces cell cycle arrest and reduces cell invasion in human ovarian cancer cells

The association of TMEM45A with various cancers has been recently reported. However, the biological function of TMEM45A in ovarian cancer remains unclear. The present study aimed to elucidate the role of TMEM45A in regulating the biological behavior of ovarian cancer cells. We compared the expression of TMEM45A between ovarian cancer tissues and normal tissues based on RNA-sequencing data of the ovarian cancer cohort from The Cancer Genome Atlas (TCGA) project and our real-time PCR data from 25 pairs of ovarian cancer and their matched non:cancerous tissue samples. The expression of TMEM45A was then suppressed in two ovarian cancer cell lines, HO-8910 and A2780, by RNA interference. Cell proliferation, cell cycle distribution, adhesion and invasive ability were then detected using the Cell Counting Kit-8 assay (CCK-8), propidium iodide (PI) staining, and cell adhesion and Transwell assays, respectively. In addition, the mRNA and protein levels of transforming growth factor-beta (TGF-beta 1 and TGF-beta 2), Ras homolog family member A (RhoA) and Rho-associated kinase 2 (ROCK2) were detected with real-time PCR and western blotting, respectively. TCGA data and our real-time PCR results demonstrated the overexpression of TMEM45A in ovarian cancer. Silencing of TMEM45A significantly inhibited cell proliferation and significantly increased the cell population in the G1 phase. Moreover, knockdown of TMEM45A also inhibited cell adhesion as well as cell invasion. More importantly, suppression of TMEM45A notably downregulated the expression of TGF-beta 1, TGF-beta 2, RhoA and ROCK2. In conclusion, TMEM45A may function as an oncogene for ovarian cancer, and inhibition of TMEM45A may be a therapeutic strategy for ovarian cancer.