CENPO regulated proliferation and apoptosis of colorectal cancer in a p53-dependent manner.

Colorectal cancer (CRC) is considered to be a leading cause of cancer-related death. Centromere protein O (CENPO) can prevent the separation of sister chromatids and cell death after spindle injury. Nevertheless, the role of CENPO in CRC has not been reported. The expression level of CENPO in CRC was revealed by TCGA database and immunohistochemical (IHC) staining. Subsequently, the loss-of-function assays were performed to identified the role of CENPO in CRC in vitro and in vivo. Our data demonstrated that CENPO was highly expressed in CRC. The expression of CENPO was positively correlated with the deterioration of CRC. Moreover, CENPO knockdown inhibited the malignant phenotypes of CRC cells, which was characterized by slowed proliferation, cycle repression at G2, promotion of apoptosis, reduced migration and weakened tumorigenesis. Furthermore, CENPO knockdown downregulated the expression of N-cadherin, Vimentin, Snail, CCND1, PIK3CA and inhibited AKT phosphorylation in CRC cells. Moreover, the function of CENPO in regulating proliferation and apoptosis depended on p53. In summary, CENPO may play a promoting role in CRC through the epithelial mesenchymal transition (EMT) and PI3K/AKT signaling pathway, which can be regarded as a molecular therapeutic target for CRC.