Abstract
Background: Octamer-binding transcription factor 4 (OCT4) is a key stem cell transcription factor involved in the development of various cancers. The role of OCT4 in ovarian cancer (OC) progression and its molecular mechanism are not fully understood.Methods: First, immunohistochemistry (IHC) assays of ovarian normal tissues, OC samples, and metastatic tissues were performed to reveal the OCT4 expression profiles. We knocked down OCT4 in two OC cell lines (SKOV3 and A2780) using a lentiviral vector and performed in vitro and in vivo experiments. OCT4 was silenced to assess the proliferation, migration, and invasion of OC cells using CCK-8, colony formation, wound healing, and Transwell asssays. In addition, a nude tumor mouse model was used for the in vivo study. Mechanistically, we demonstrated that OCT4 influenced protein expression in the phosphoinositol 3-kinase (PI3K)/AKT/mTOR pathway and epithelial-mesenchymal transition (EMT)-related proteins by Western blotting and immunofluorescence (IF) assays.Results: OCT4 expression was significantly upregulated in OC samples and metastatic tissues. OCT4 silencing notably inhibited the proliferation, migration, and invasion of OC cells in vitro and in vivo. Moreover, the expression of p-PI3K, p-AKT, and p-mTOR was downregulated after OCT4 knockdown. EMT in OC samples was enhanced by OCT4.Conclusions: Our study shows that OCT4 promotes the proliferation, migration, and invasion of OC cells by participating in the PI3K/AKT/mTOR signaling axis, suggesting that it could serve as a potential therapeutic target for OC patients.