Stk32C, a member of the serine/threonine protein kinase of AGC superfamily, was first found highly expressed in brain tissues. It may play roles in multiple biological processes, though its exact function remains to be fully elucidated. Some studies suggest its possible involvement in pathways related to cell proliferation, migration, and invasion, as well as in glycolysis regulation [3,2].

In cancer research, data from TCGA database showed that the Stk32C gene is overexpressed in bladder cancer and a number of other human tumors. Slicing of Stk32C inhibited tumor cell proliferation, migration and invasion in vitro, and knocking-down of Stk32C restricted the growth of tumor cells in mice, indicating its promoting role in tumor progression [3]. In triple-negative breast cancer, elevated Stk32C expression was associated with unfavorable prognosis in doxorubicin-treated patients. Depletion of Stk32C augmented the sensitivity of doxorubicin-resistant cells to doxorubicin, with the cytoplasmic subset of Stk32C mediating this effect mainly through glycolysis regulation [2].

In conclusion, Stk32C appears to be involved in cancer-related processes such as tumor cell growth, invasion, and drug resistance, especially in bladder and triple-negative breast cancers. Its role in these diseases highlights the potential of targeting Stk32C as a new therapeutic approach. Additionally, its association with other conditions like intellectual disability and mental disorders from methylation-related studies suggests a broader influence on human health, although further research is needed to fully understand its functions [1,4,5].