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• W1975667915 endingPage "745" @default.
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• W1975667915 abstract "Summary The p16 INK4a ‐Rb tumour suppressor pathway is required for the initiation and maintenance of cellular senescence, a state of permanent growth arrest that acts as a natural barrier against cancer progression. Senescence can be overcome if the pathway is not fully engaged, and this may occur when p16 INK4a is inactivated. p16 INK4a is frequently altered in human cancer and germline mutations affecting p16 INK4a have been linked to melanoma susceptibility. To characterize the functions of melanoma‐associated p16 INK4a mutations, in terms of promoting proliferative arrest and initiating senescence, we utilized an inducible expression system in a melanoma cell model. We show that wild‐type p16 INK4a promotes rapid cell cycle arrest that leads to a senescence programme characterized by the appearance of chromatin foci, activation of acidic β‐galactosidase activity, p53 independence and Rb dependence. Accumulation of wild‐type p16 INK4a also promoted cell enlargement and extensive vacuolization independent of Rb status. In contrast, the highly penetrant p16 INK4a variants, R24P and A36P failed to arrest cell proliferation and did not initiate senescence. We also show that overexpression of CDK4, or its homologue CDK6, but not the downstream kinase, CDK2, inhibited the ability of wild‐type p16 INK4a to promote cell cycle arrest and senescence. Our data provide the first evidence that p16 INK4a can initiate a CDK4/6‐dependent autonomous senescence programme that is disabled by inherited melanoma‐associated mutations." @default.
• W1975667915 created "2016-06-24" @default.
• W1975667915 creator A5025256131 @default.
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• W1975667915 creator A5062978331 @default.
• W1975667915 creator A5069277796 @default.
• W1975667915 date "2008-09-17" @default.
• W1975667915 modified "2023-10-16" @default.
• W1975667915 title "p16^INK4a-induced senescence is disabled by melanoma-associated mutations" @default.
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• W1975667915 doi "https://doi.org/10.1111/j.1474-9726.2008.00422.x" @default.
• W1975667915 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2582406" @default.
• W1975667915 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18843795" @default.
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