Tumor markers of bladder cancer (BC) have been investigated for many years, but the clinical treatment based on these biomarkers is still unsatisfactory. STK32C, a member of the serine/threonine protein kinase of AGC superfamily, was first found to be highly expressed in brain tissues; however, the role of STK32C in malignant disease has not been determined. Data from TCGA database showed that the STK32C gene is overexpressed in BC and a number of other human tumors. In the current study, immunohistochemistry revealed that high expression of STK32C protein in tumor tissues was significantly associated with poor clinico pathologic features and a short relapse-free survival (RFS) in patients with BC. Slicing of STK32C inhibited tumor cell proliferation, migration and invasion in vitro. In vivo animal experiments demonstrated that knocking-down of STK32C restricted the growth of tumor cells in mice. Finally, microarray analysis revealed that silencing of STK32C inhibited the activity of the HMGB1 pathway and regulated the expression of key genes in this pathway. In conclusion, our study showed novel promoting roles for STK32C in human tumors, which may provide a new therapeutic target for the patients with BC.
Keywords: STK32C; TCGA; bladder cancer; progression; protein kinase.