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    Reduction of total E2F/DP activity induces senescence-like cell cycle arrest in cancer cells lacking functional pRB and p53.

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    Authors
    Maehara, Kayoko
    Yamakoshi, Kimi
    Ohtani, Naoko
    Kubo, Yoshiaki
    Takahashi, Akiko
    Arase, Seiji
    Jones, Nic
    Hara, Eiji
    Affiliation
    Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Manchester M20 4BX, England, UK.
    Issue Date
    2005-02-14
    
    Metadata
    Show full item record
    Abstract
    E2F/DP complexes were originally identified as potent transcriptional activators required for cell proliferation. However, recent studies revised this notion by showing that inactivation of total E2F/DP activity by dominant-negative forms of E2F or DP does not prevent cellular proliferation, but rather abolishes tumor suppression pathways, such as cellular senescence. These observations suggest that blockage of total E2F/DP activity may increase the risk of cancer. Here, we provide evidence that depletion of DP by RNA interference, but not overexpression of dominant-negative form of E2F, efficiently reduces endogenous E2F/DP activity in human primary cells. Reduction of total E2F/DP activity results in a dramatic decrease in expression of many E2F target genes and causes a senescence-like cell cycle arrest. Importantly, similar results were observed in human cancer cells lacking functional p53 and pRB family proteins. These findings reveal that E2F/DP activity is indeed essential for cell proliferation and its reduction immediately provokes a senescence-like cell cycle arrest.
    Citation
    Reduction of total E2F/DP activity induces senescence-like cell cycle arrest in cancer cells lacking functional pRB and p53. 2005, 168 (4):553-60 J. Cell Biol.
    Journal
    The Journal of Cell Biology
    URI
    http://hdl.handle.net/10541/75660
    DOI
    10.1083/jcb.200411093
    PubMed ID
    15716376
    Type
    Article
    Language
    en
    ISSN
    0021-9525
    ae974a485f413a2113503eed53cd6c53
    10.1083/jcb.200411093
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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