GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors

oleh: Aslamuzzaman Kazi, Shengyan Xiang, Hua Yang, Daniel Delitto, José Trevino, Rays H. Y. Jiang, Muhammad Ayaz, Harshani R. Lawrence, Perry Kennedy, Saïd M. Sebti

Format: Article
Diterbitkan: Nature Portfolio 2018-12-01

Deskripsi

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.