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

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 o...

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Veröffentlicht in:Genes & development 1998-08, Vol.12 (16), p.2469-2474
Hauptverfasser: Robles, A I, Rodriguez-Puebla, M L, Glick, A B, Trempus, C, Hansen, L, Sicinski, P, Tennant, R W, Weinberg, R A, Yuspa, S H, Conti, C J
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Sprache:eng
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Zusammenfassung: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.
ISSN:0890-9369
1549-5477
DOI:10.1101/gad.12.16.2469