TMEM61 Promotes Malignant Behaviors and Maintains Genomic Stability in Ovarian Cancer Cells.

Abstract

Background: Transmembrane protein 61 (TMEM61) has previously been reported in several malignancies. However, its function in ovarian cancer remains unclear. Here, we aimed to investigate the role and underlying mechanisms of TMEM61 in ovarian cancer cells.

Methods: Differentially expressed genes were identified by analyzing transcriptomic data of 426 ovarian cancer tissues from The Cancer Genome Atlas database and 88 normal ovarian tissues from the Genotype-Tissue Expression database using the web-based analytical tool GEPIA2. The effects of TMEM61 knockdown on ovarian cancer cell invasion, migration, and proliferation were evaluated using Transwell, wound healing, and Cell Counting Kit-8 assays. The effect of TMEM61 knockdown on DNA damage and cytosolic DNA accumulation was assessed using immunofluorescence and comet assays. TMEM61 and programmed death-ligand 1 (PD-L1) expression levels were assessed using immunoblotting and reverse transcription-quantitative polymerase chain reaction.

Results: TMEM61 exhibited very low expression in normal ovarian tissues, but its expression was significantly upregulated in ovarian cancer tissues. TMEM61 knockdown significantly inhibited the proliferation, migration, and invasion of ovarian cancer cells; induced DNA damage and cytoplasmic DNA accumulation; and upregulated PD-L1 expression in ovarian cancer cells.

Conclusions: TMEM61 promotes malignant behavior and maintains genomic stability in ovarian cancer cells. TMEM61 may serve as a potential biomarker and molecular target for ovarian cancer.