Nature Communications (Dec 2018)

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

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

DOI
https://doi.org/10.1038/s41467-018-07644-6
Journal volume & issue
Vol. 9, no. 1
pp. 1 – 9

Abstract

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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.