APOC1 inhibit NKTCL doxorubicin sensitivity by promoting mitophagy.

NKTCL is a highly aggressive malignant tumor, especially prevalent in the southern regions of China. Although chemotherapy regimens based on ADM have achieved certain therapeutic effects in early treatment, the issue of ADM resistance severely limits the therapeutic efficacy and makes it difficult to improve patient survival rates. Our research results indicate that the expression level of APOC1 is closely related to the sensitivity of NKTCL cells to ADM. The upregulation of APOC1 may promote mitophagy, clear damaged mitochondria, stabilize the intracellular environment, and enhance the tolerance of tumor cells to ADM. Furthermore, APOC1 may further affect the formation of mitophagy and drug resistance by activating specific signaling pathways, such as the STAT3 signaling pathway. Animal experiments further confirm the conclusions of in vitro experiments, showing that APOC1 regulates mitophagy through p-STAT3^Tyr705, thereby promoting the drug resistance of NKTCL. These findings provide a new perspective for the development of novel therapeutic strategies targeting APOC1 and its associated signaling pathways, which may help overcome the issue of ADM resistance in NKTCL.