CDCA2 Promotes HCC Cells Development via AKT-mTOR Pathway.

Abstract

Hepatocellular carcinoma (HCC) is a highly aggressive and solid malignancy with a poor prognosis. Cell division cycle associated 2 (CDCA2) is highly expressed in HCC and is considered to be closely related to the prognosis of patients with HCC. In this research, we aimed to investigate the function and potential mechanism of CDCA2 in HCC cells. Gain- and loss-of-function experiments were conducted to determine the biological function of CDCA2 in HCC cells. Quantitative reverse transcription-polymerase chain reaction and western blot were utilized to examine the Messenger RNA (mRNA) and protein levels of CDCA2 in HCC cells. The malignant behaviors of HCC cells were analyzed by several biological experiments including cell viability, cell colony formation, and transwell assays. Western blot was also implemented to examine the expression of : AKT, protein kinase B and mTOR, mammalian target of rapamycin (AKT-mTOR) pathway related proteins and Cyclin D1. A significant increase of CDCA2 was observed in HCC cell lines. Upregulation of CDCA2 resulted in the enhancement of the growth, migration, and invasion of HCC cells. Inversely, depletion of CDCA2 displayed the opposite results. Furthermore, the protein levels of p-AKT, p-mTOR, and Cyclin D1 were elevated with CDCA2 upregulation and reduced with CDCA2 depletion in HCC cells. Our observations revealed that CDCA2 promoted the malignant development of HCC cells, and AKT-mTOR pathway might involve in the underlying mechanism.