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Role of the alternative INK4A proteins in human keratinocyte senescence: Evidence for the specific inactivation of p16(INK4A) upon immortalization

  1. Author:
    Munro, J.
    Stott, F. J.
    Vousden, K. H.
    Peters, G.
    Parkinson, E. K.

  2. Author Address

    Parkinson EK Beatson Inst Canc Res, Canc Res Campaign, Beatson Labs Garscube Estate,Switchback Rd Glasgow G61 1BD Lanark Scotland Beatson Inst Canc Res, Canc Res Campaign, Beatson Labs Glasgow G61 1BD Lanark Scotland Imperial Canc Res Fund Labs London WC2A 3PX England NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program Frederick, MD 21702 USA
    1. Year: 1999
  2. Journal: Cancer Research
    1. 59
    2. 11
    3. Pages: 2516-2521
  4. Type of Article: Article
  1. Abstract:

    The INK4A locus on human chromosome 9p21 encodes two genes that have been implicated in replicative senescence and tumor suppression, p16(INK4A) and p14(ARF). In contrast to p16(INK4A), Which is up-regulated to high levels, we were unable to detect p(14ARF) protein in senescent human keratinocytes. Also, p53, an established target of p14(ARF), did not increase, suggesting that p14(ARF) is not instrumental in human keratinocyte senescence,In neoplastic keratinocyte cultures, p16(INK4A) inactivation was invariably associated With the immortal phenotype, and there,vas evidence for the inactivation of p(16INK4A), independent of p14(ARF) in 6 of 10 lines that lacked large homozygous deletions. In contrast, we failed to detect exon Ip mutations or p16(INK4A)-independent deletions. These results emphasize the previously proposed role for p16(INK4A) in human keratinocyte senescence but do not rule out a supporting role for p14(ARF) inactivation. [References: 20]

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