The disulfidptosis form of cell death, which was previously unknown, is described in a study from the University of Texas MD Anderson Cancer Center that was published today in Nature Cell Biology. This finding may pave the way for fresh cancer treatment options. As described in the study, disulfidptosis is triggered when cells with high levels of the SLC7A11 protein are subjected to glucose starvation. In preclinical models, treatment with glucose inhibitors induced disulfidptosis in cancer cells with high SLC7A11 expression, effectively suppressing tumor growth without significant toxicity in normal tissues. The study was led by Boyi Gan, Ph.D., and Junjie Chen, Ph.D., both professors of Experimental Radiation Oncology. “Cancer cells rely on SLC7A11 to import cystine for maintaining redox balance and for cell survival. However, this also exposes an Achilles heel in SLC7A11-high cancer cells because these cells are dependent on glucose to resolve their disulfide-overloading issue,” Gan said. “Starving these cells of glucose can overwhelm them with toxic disulfide molecules, resulting in rapid cell death.”