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 language | English (US) |
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Pages (from-to) | 2469-2474 |
Number of pages | 6 |
Journal | Genes and Development |
Volume | 12 |
Issue number | 16 |
DOIs | |
State | Published - Aug 15 1998 |
All Science Journal Classification (ASJC) codes
- Genetics
- Developmental Biology