JS-K enhances renal cell carcinoma radiosensitivity through the Wnt/β-catenin signaling pathway and inhibits DNA damage repair.

The study investigated the effect of the glutathione S-transferase-activated nitric oxide donor JS-K [O2-(2,4-dinitrophenyl)1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate] to enhance the sensitivity of renal cancer cells to radiation therapy. JS-K has shown promising anti-tumor effects in various types of tumors; however, research on its role in cancer radioresistance is limited. The traditional concept is that renal cell carcinoma (RCC) has inherent resistance to radiation.

JS-K induces ferroptosis in renal carcinoma cells by regulating the c-Myc-GSTP1 Axis.

JS-K is a precursor drug of nitric oxide (NO) and inhibits tumor growth through various mechanisms. Ferroptosis, a form of cell death closely related to lipid peroxidation, is increasingly being recognized for its role in cancer biology. However, the relevance of ferroptosis in the anti-tumor effects of JS-K is yet to be defined.