Targeting glutamine metabolism sensitizes pancreatic cancer to PARP-driven metabolic catastrophe induced by ß-lapachone.

CONCLUSIONS: This treatment strategy illustrates proof of principle that simultaneously decreasing glutamine metabolism-dependent tumor anti-oxidant defenses and inducing supra-physiological ROS formation are tumoricidal and that this rationally designed combination strategy lowers the required doses of both agents in vitro and in vivo. The non-overlapping specificities of GLS1 inhibitors and ß-lap for PDA tumors afford high tumor selectivity, while sparing normal tissue.
PMID: 26462257 [PubMed]

Source: Diabetes Metab - October 16, 2015 Category: Endocrinology Authors: Chakrabarti G, Moore ZR, Luo X, Ilcheva M, Ali A, Padanad M, Zhou Y, Xie Y, Burma S, Scaglioni PP, Cantley LC, DeBerardinis RJ, Kimmelman AC, Lyssiotis CA, Boothman DA Tags: Cancer Metab Source Type: research