Silencing of synaptotagmin 13 inhibits tumor growth through suppressing proliferation and promoting apoptosis of colorectal cancer cells.

Abstract

The treatment of colorectal cancer is currently hampered by the lack of early detection technology. The identification of molecular biomarkers for colorectal cancer is crucial for improving prognosis. Synaptotagmin (SYT) 13 has been reported to be associated with several human tumors, but its role in colorectal cancer remains elusive. In the present study, immunohistochemistry was utilized to detect the expression of SYT13 in colorectal cancer tissues and cells. MTT, colony formation, wound healing and Transwell assays were conducted to evaluate the effect of SYT13 knockdown on the biological behavior of RKO and HCT116 cells. Cell apoptosis and cell cycle profiles were detected by FACS. A mouse xenograft model was constructed to investigate the effect of SYT13 on colorectal cancer in vivo. The results indicated that SYT13 was upregulated in colorectal tumor tissues compared with paracancerous tissues. Silencing of SYT13 inhibited the proliferation, colony formation, migration and invasion ability of RKO and HCT116 cells. Moreover, SYT13 knockdown arrested the cell cycle in the G2 phase, thus inducing cell apoptosis. The in vivo experiments also demonstrated the inhibitory effect of SYT13 on tumor growth. In conclusion, the present study demonstrated that SYT13 may act as a promoter in the development and progression of colorectal cancer and, therefore, may be of value as a target for the development of novel treatment strategies.