A CRAF/glutathione-S-transferase P1 complex sustains autocrine growth of cancers with <i>KRAS</i> and <i>BRAF</i> mutations

Abstract

Significance A strategy to overcome therapeutic obstacles of m KRAS and m BRAF cancers is devised based on the finding, here, that the RAF/MEK/ERK cascade is by-passed by an autocrine signal loop established by interaction of CRAF with GSTP1. The interaction evokes stabilization of CRAF from proteosomal degradation and facilitation of RAF-dimer formation. Thus, blocking CRAF/GSTP1 interactions should generate additive antiproliferative effects.