CIP2A is overexpressed in human endometrioid adenocarcinoma and regulates cell proliferation, invasion and apoptosis

Abstract

ObjectiveCancerous inhibitor of protein phosphatase 2A (CIP2A) is a recently identified oncoprotein that stabilizes c-Myc and promotes cell proliferation and transformation. Here, we investigated the clinical significance and biological function of CIP2A in endometrial cancer. MethodCIP2A expression was assessed in normal endometrium, endometrial hyperplasia, endometrial atypical hyperplasia, and endometrioid adenocarcinoma tissues using immunohistochemistry, western blot, and RT-PCR. The effect of reduced CIP2A expression was assessed by siRNA knockdown in Ishikawa and An3ca endometrial cell lines. The roles of CIP2A in proliferation, apoptosis, and the cell cycle were assessed using CCK-8 assays, colony formation assays, and flow cytometry, respectively. ResultsOur results show that CIP2A expression was higher in endometrioid adenocarcinoma tissues and cell lines. Furthermore, CIP2A siRNA significantly reduced the proliferation rate and invasion of Ishikawa and An3ca cells, and induced a significant level of apoptosis in Ishikawa cells. Moreover, CIP2A depletion resulted in reduced c-Myc and cyclin D1 protein levels, and increased caspase-3 expression. ConclusionsCIP2A is overexpressed in endometrioid adenocarcinoma and CIP2A promotes the malignant growth and invasion,decrease apoptosis in entometrioid adenocarcinoma cell lines. These results validate that CIP2A plays an important role in the carcinogenesis of endometrioid adenocarcinoma and establishes CIP2A as a clinically relevant oncoprotein and may presents a promising therapeutic target for cancer treatment.