YAP1 takes over when oncogenic K-Ras slumbers

Cell. 2014 Jul 3;158(1):11-2. doi: 10.1016/j.cell.2014.06.021.

Abstract

It is of great therapeutic importance to understand why tumors relapse after the failure of therapies targeting oncogenes to which cancer cells are addicted. In this issue, Kapoor et al. and Shao et al. identify the transcriptional coactivator YAP1 as a central driver of compensation for the loss of K-Ras signaling in K-Ras-dependent cancers.

Publication types

  • Comment

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism*
  • Adenocarcinoma / metabolism*
  • Animals
  • Carcinoma, Pancreatic Ductal / metabolism*
  • Cell Cycle Proteins
  • Cell Survival*
  • Colonic Neoplasms / drug therapy*
  • Drug Resistance, Neoplasm*
  • Epithelial-Mesenchymal Transition*
  • Humans
  • Lung Neoplasms / drug therapy*
  • Pancreatic Neoplasms / metabolism*
  • Phosphoproteins / metabolism*
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins p21(ras) / metabolism*
  • Transcription Factors
  • YAP-Signaling Proteins
  • ras Proteins / metabolism*

Substances

  • Adaptor Proteins, Signal Transducing
  • Cell Cycle Proteins
  • KRAS protein, human
  • Phosphoproteins
  • Proto-Oncogene Proteins
  • Transcription Factors
  • YAP-Signaling Proteins
  • YAP1 protein, human
  • Yap1 protein, mouse
  • Hras protein, mouse
  • Proto-Oncogene Proteins p21(ras)
  • ras Proteins