Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer

Abstract

SUMMARYCancer cell survival upon cytotoxic drug exposure leads to changes in cell identity, dictated by the epigenome. Several metabolites serve as substrates or co-factors to chromatin-modifying enzymes, suggesting that metabolic changes can underlie change in cell fate. Here, we show that progression of triple-negative breast cancer (TNBC) to taxane-resistance is characterized by altered methionine metabolism and S-adenosylmethionine (SAM) availability, giving rise to

Serine and Methionine Metabolism: Vulnerabilities in Lethal Prostate Cancer

“…These findings extend the cancer contexts in which this mechanism has been attributed to the pathogenesis of cancer. Previous reports have identified similar SGOC pathway-mediated epigenetic alterations upon loss of LKB1 in a type of pancreatic cancer (Kottakis et al, 2016) and the evolution of chemoresistance in breast cancer (Deblois et al, 2018).…”