Nature Communications (Dec 2018)
GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors
Abstract
Direct targeting of mutant KRas is challenging and alternative approaches are needed. Here they show glycogen synthase kinase 3 (GSK3) to be required for the growth and survival of human mutant KRas-dependent tumors but dispensable for mutant KRas-independent tumors and show GSK3 inhibition to inhibit in vivo growth of Kras mutant patient-derived pancreatic tumors.