STK32C modulates doxorubicin resistance in triple-negative breast cancer cells via glycolysis regulation.

Understanding the mechanisms underlying doxorubicin resistance in triple-negative breast cancer (TNBC) holds paramount clinical significance. In our study, we investigate the potential of STK32C, a little-explored kinase, to impact doxorubicin sensitivity in TNBC cells. Our findings reveal elevated STK32C expression in TNBC specimens, associated with unfavorable prognosis in doxorubicin-treated TNBC patients. Subsequent experiments highlighted that STK32C depletion significantly augmented the sensitivity of doxorubicin-resistant TNBC cells to doxorubicin. Mechanistically, we unveiled that the cytoplasmic subset of STK32C plays a pivotal role in mediating doxorubicin sensitivity, primarily through the regulation of glycolysis. Furthermore, the kinase activity of STK32C proved to be essential for its mediation of doxorubicin sensitivity, emphasizing its role as a kinase. Our study suggests that targeting STK32C may represent a novel therapeutic approach with the potential to improve doxorubicin's efficacy in TNBC treatment.