Ovarian cancer is the third most common malignancy in the gynecological reproductive system. Epithelial ovarian cancer (EOC) represents one of the most common subtypes of ovarian cancer. Once diagnosed, the treatment strategies for EOC are limited, and the prognosis is often poor. Recently, inositol monophosphatase 2 (IMPA2) was found to act as an oncogene in cancer development. However, the role of IMPA2 in EOC is unclear. In the present study, the role of IMPA2 in EOC development was assessed through numerous experiments, including knockdown and MTT assays; multiparametric high-content screening; colony formation, apoptosis and Transwell assays, and a xenografted mouse model. IMPA2 was shown to be critical for EOC cell proliferation, growth, migration and tumorigenesis. In addition, experiments showed that knockdown of IMPA2 expression significantly suppressed proliferation and colony formation in the ES-2 and SKOV3 cell lines in vitro. IMPA2 knockdown also suppressed the migration and invasion of the EOC cell lines, and apoptosis was induced. In vivo, IMPA2 knockdown reduced the tumorigenesis of the EOC cells. Mechanistically, IMPA2 knockdown suppressed the AKT/mTOR signaling pathway and epithelial-mesenchymal transition (EMT). Collectively, the results from the present study demonstrated that IMPA2 may be a novel oncogene in EOC cells via regulation of the AKT/mTOR pathway and EMT.
Keywords: AKT/mTOR; epithelial ovarian cancer; epithelial-mesenchymal transition; inositol monophosphatase 2; tumorigenesis.
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