CD44 promotes Kras-dependent lung adenocarcinoma

P. Zhao, M. S. Damerow, P. Stern, A. H. Liu, A. Sweet-Cordero, K. Siziopikou, J. R. Neilson, P. A. Sharp, C. Cheng*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

Kras-induced non-small-cell lung adenocarcinoma is the major subtype of lung cancers and is associated with poor prognosis. Using a lung cancer mouse model that expresses a cre-mediated Kras G12D mutant, we identified a critical role for the cell surface molecule CD44 in mediating cell proliferation downstream of oncogenic Kras signaling. The deletion of CD44 attenuates lung adenocarcinoma formation and prolongs the survival of these mice. Mechanistically, CD44 is required for the activation of Kras-mediated signaling through the mitogen-activated protein kinase (MAPK) pathway and thus promotes tumor cell proliferation. Together, these results reveal an unrecognized role for CD44 in oncogenic Kras-induced lung adenocarcinoma and suggest that targeting CD44 could be an effective strategy for halting Kras-dependent carcinomas.

Original languageEnglish (US)
Pages (from-to)5186-5190
Number of pages5
JournalOncogene
Volume32
Issue number43
DOIs
StatePublished - 2013

Keywords

  • CD44
  • Kras
  • lung adenocarcinoma

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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