Recharacterization of the Tumor Suppressive Mechanism of RSL3 Identifies the Selenoproteome as a Druggable Pathway in Colorectal Cancer

Abstract

Chemoproteomic profiling reveals that RSL3 functions through pan-selenoprotein inhibition beyond GPX4 and identifies ALKBH8, a tRNA-selenocysteine methyltransferase essential for selenoprotein translation, as a therapeutic target to disrupt redox balance in colorectal cancer. See related commentary by Short, p. 2775.