Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo

Ana I. Robles, Marcelo L. Rodriguez-Puebla, Adam B. Glick, Carol Trempus, Laura Hansen, Piotr Sicinski, Raymond W. Tennant, Robert A. Weinberg, Stuart H. Yuspa, Claudio J. Conti

Research output: Contribution to journalArticlepeer-review

196 Scopus citations

Abstract

Cyclin D1 is part of a cell cycle control node consistently deregulated in most human cancers. However, studies with cyclin D1-null mice indicate that it is dispensable for normal mouse development as well as cell growth in culture. Here, we provide evidence that ras-mediated tumorigenesis depends on signaling pathways that act preferentially through cyclin D1. Cyclin D1 expression and the activity of its associated kinase are up-regulated in keratinocytes in response to oncogenic ras. Furthermore, cyclin D1 deficiency results in up to an 80% decrease in the development of squamous tumors generated through either grafting of retroviral ras-transduced keratinocytes, phorbol ester treatment of ras transgenic mice, or two-stage carcinogenesis.

Original languageEnglish (US)
Pages (from-to)2469-2474
Number of pages6
JournalGenes and Development
Volume12
Issue number16
DOIs
StatePublished - Aug 15 1998

All Science Journal Classification (ASJC) codes

  • Genetics
  • Developmental Biology

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