A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells

Nitric oxide (NO) works as a signaling molecule, toxicant, and antioxidant in the body's physiological and pathological processes. JS-K is designed to be activated by glutathione-S-transferase (GST) and release NO in a sustained and controlled manner within the tumor cells. JS-K also promotes apoptosis in cancer cells through mitogen-activated protein kinase (MAPK) pathway, ubiquitin-proteasome pathway, cell factor β-catenin/T (TCF) signaling pathway, and other mechanisms. In future studies, we should further develop new NO precursors, so that new drugs in the treatment of cancer can become more efficient, more accurate, and have less adverse reactions.