STK32C, a member of the serine/threonine protein kinase of AGC superfamily, was first found highly expressed in brain tissues [2]. Its exact function remains somewhat elusive, but it has been implicated in multiple biological processes. Kinome analysis indicated it may be involved in insulin signaling, with impaired phosphorylation sites in T2D potentially due to reduced action of STK32C among other kinases [3].

In triple-negative breast cancer (TNBC), elevated STK32C expression is associated with unfavorable prognosis in doxorubicin-treated patients. Depletion of STK32C enhanced the sensitivity of doxorubicin-resistant TNBC cells to doxorubicin, with the cytoplasmic subset of STK32C regulating glycolysis to mediate doxorubicin sensitivity [1]. In bladder cancer, STK32C is overexpressed. Slicing of STK32C inhibited tumor cell proliferation, migration and invasion in vitro, and knocking-down restricted tumor cell growth in mice. Microarray analysis revealed that silencing of STK32C inhibited the HMGB1 pathway [2].

In summary, STK32C appears to play significant roles in cancer-related processes such as drug resistance in TNBC and tumor progression in bladder cancer. Its involvement in insulin signaling also indicates a potential link to metabolic diseases. Understanding STK32C through model-based research, like the in vitro and in vivo experiments in cancer studies, provides insights into disease mechanisms and may offer new therapeutic targets for these diseases.