Expression of securin promotes colorectal cancer cell death via a p53-independent pathway after radiation.

Securin has been shown to regulate genomic stability; nevertheless, the role of securin on the cytotoxicity after radiation is still unclear. Exposure to 1-10 Gy X-ray radiation induced cell death in RKO colorectal cancer cells. The protein levels of securin, p53, and p21 were elevated by radiation. The proteins of phosphorylation of p53 at serine-15, which located on the nuclei of cancer cells, were highly induced by radiation. However, radiation increased securin proteins, which located on both of nuclei and cytoplasma in RKO cells. The p53-wild type colorectal cancer cells were more susceptible on cytotoxicity than the p53-mutant cells following exposure to radiation. Besides, the existence of securin in colorectal cancer cells induced higher apoptosis than the securin-null after radiation. Securin proteins were elevated by radiation in the p53-wild type and -mutant cells; furthermore, radiation raised the p53 protein expression in both the securin-wild type and -null cells. As a whole, these findings suggest that the existence of securin promotes apoptosis via a p53-indpendent pathway after radiation in human colorectal cancer cells.