STK32C, a member of the serine/threonine protein kinase of AGC superfamily, was first found highly expressed in brain tissues. Its biological function was once unknown, but recent research has associated it with multiple important biological processes. It may be involved in kinase-related pathways and could potentially play a role in regulating various cellular functions [3,2].

In triple-negative breast cancer (TNBC), STK32C depletion significantly augmented the sensitivity of doxorubicin-resistant TNBC cells to doxorubicin, with the cytoplasmic subset of STK32C mediating this effect mainly through glycolysis regulation [1]. In bladder cancer, 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 in vivo, while also inhibiting the activity of the HMGB1 pathway [2].

In conclusion, STK32C is a kinase that appears to play a role in cancer-related processes, particularly in modulating drug resistance in TNBC and promoting tumor progression in bladder cancer. Understanding the function of STK32C through in vivo studies like those in mouse models can potentially provide new therapeutic targets for these cancers.