Sam68 reduces cisplatin-induced apoptosis in tongue carcinoma

Background: resistance to anticancer agents is a major obstacle for successful chemotherapy in tongue squamous cancer. sam68 is an oncogenic-related protein in oral tongue squamous cell carcinoma functions as a signaling molecule mediating apoptosis,whose over-expression is associated with the clinicopathologic characteristics and prognosis of patients. the present study was to examine the effect of sam68 on chemotherapeutics-induced apoptosis in oral tongue squamous cell carcinoma,and its clinical significance in oral tongue squamous cell carcinoma progression. methods: the effect of sam68 on apoptosis induced by cisplatin was examined both in vitro and in vivo,using annexin v staining and terminal deoxynucleotidyl transferase-mediated dutp nick end labeling assays. real-time pcr and western blotting analysis were used to detect mrna and protein expression levels. results: upregulation of sam68 significantly inhibited cisplatin-induced apoptosis in oral tongue squamous cell carcinoma cells,associated with induction of anti-apoptotic proteins caspase-9,caspase-3,and parp. in contrast,silencing sam68 expression significantly enhanced the sensitivity of oral tongue squamous cell carcinoma cells to apoptosis induced by cisplatin both in vitro and in vivo. conclusions: the current study suggests that sam68 could enhance the anti-apoptosis activity of oral tongue squamous cell carcinoma cells. sam68 is a potential pharmacologic target for the treatment of oral tongue squamous cell carcinoma and inhibition of sam68 expression might represent a novel strategy to sensitize oral tongue squamous cell carcinoma to chemotherapy. © 2016 the author(s).