Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7

Cell. 2008 Feb 8;132(3):363-74. doi: 10.1016/j.cell.2007.12.032.

Abstract

Expression of an oncogene in a primary cell can, paradoxically, block proliferation by inducing senescence or apoptosis through pathways that remain to be elucidated. Here we perform genome-wide RNA-interference screening to identify 17 genes required for an activated BRAF oncogene (BRAFV600E) to block proliferation of human primary fibroblasts and melanocytes. Surprisingly, we find a secreted protein, IGFBP7, has a central role in BRAFV600E-mediated senescence and apoptosis. Expression of BRAFV600E in primary cells leads to synthesis and secretion of IGFBP7, which acts through autocrine/paracrine pathways to inhibit BRAF-MEK-ERK signaling and induce senescence and apoptosis. Apoptosis results from IGFBP7-mediated upregulation of BNIP3L, a proapoptotic BCL2 family protein. Recombinant IGFBP7 (rIGFBP7) induces apoptosis in BRAFV600E-positive human melanoma cell lines, and systemically administered rIGFBP7 markedly suppresses growth of BRAFV600E-positive tumors in xenografted mice. Immunohistochemical analysis of human skin, nevi, and melanoma samples implicates loss of IGFBP7 expression as a critical step in melanoma genesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Substitution
  • Animals
  • Apoptosis*
  • Autocrine Communication
  • Cell Line, Tumor
  • Cell Proliferation
  • Cellular Senescence*
  • Fibroblasts / cytology
  • Humans
  • Insulin-Like Growth Factor Binding Proteins / genetics
  • Insulin-Like Growth Factor Binding Proteins / metabolism*
  • MAP Kinase Signaling System
  • Melanocytes / cytology
  • Melanocytes / metabolism
  • Melanoma / genetics
  • Melanoma / metabolism
  • Membrane Proteins / metabolism
  • Mice
  • Neoplasm Transplantation
  • Nevus, Pigmented / metabolism
  • Paracrine Communication
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins B-raf / genetics
  • Proto-Oncogene Proteins B-raf / metabolism*
  • RNA Interference
  • Recombinant Proteins / genetics
  • Recombinant Proteins / metabolism
  • Transplantation, Heterologous
  • Tumor Suppressor Proteins / metabolism
  • Up-Regulation

Substances

  • BNIP3L protein, human
  • Insulin-Like Growth Factor Binding Proteins
  • Membrane Proteins
  • Proto-Oncogene Proteins
  • Recombinant Proteins
  • Tumor Suppressor Proteins
  • insulin-like growth factor binding protein-related protein 1
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf