FAK to the rescue: activated stroma promotes a "safe haven" for BRAF-mutant melanoma cells by inducing FAK signaling

Cancer Cell. 2015 Apr 13;27(4):429-31. doi: 10.1016/j.ccell.2015.03.013.


Perhaps the most pressing need in cancer therapeutics is to understand drug resistance. In this issue of Cancer Cell, Hirata and colleagues show that melanoma-associated fibroblasts can drive resistance to the BRAF inhibitor PLX4720 by stimulating matrix production/remodeling, and, consequently, survival signaling in melanoma cells via β1-integrin, Src, and FAK.

Publication types

  • Comment

MeSH terms

  • Animals
  • Drug Resistance, Neoplasm*
  • Focal Adhesion Protein-Tyrosine Kinases / metabolism*
  • Humans
  • Integrin beta1 / metabolism*
  • Melanoma / metabolism*
  • Proto-Oncogene Proteins B-raf / antagonists & inhibitors*
  • Tumor Microenvironment*


  • Integrin beta1
  • Focal Adhesion Protein-Tyrosine Kinases
  • Proto-Oncogene Proteins B-raf