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P16(INK4a) translation suppressed by miR-24.


ABSTRACT: Expression of the tumor suppressor p16(INK4a) increases during aging and replicative senescence.Here, we report that the microRNA miR-24 suppresses p16 expression in human diploid fibroblasts and cervical carcinoma cells. Increased p16 expression with replicative senescence was associated with decreased levels of miR-24, a microRNA that was predicted to associate with the p16 mRNA coding and 3'-untranslated regions. Ectopic miR-24 overexpression reduced p16 protein but not p16 mRNA levels. Conversely, introduction of antisense (AS)-miR-24 blocked miR-24 expression and markedly enhanced p16 protein levels, p16 translation, and the production of EGFP-p16 reporter bearing the miR-24 target recognition sites.Together, our results suggest that miR-24 represses the initiation and elongation phases of p16 translation.

SUBMITTER: Lal A 

PROVIDER: S-EPMC2274865 | biostudies-literature | 2008 Mar

REPOSITORIES: biostudies-literature

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<h4>Background</h4>Expression of the tumor suppressor p16(INK4a) increases during aging and replicative senescence.<h4>Methodology/principal findings</h4>Here, we report that the microRNA miR-24 suppresses p16 expression in human diploid fibroblasts and cervical carcinoma cells. Increased p16 expression with replicative senescence was associated with decreased levels of miR-24, a microRNA that was predicted to associate with the p16 mRNA coding and 3'-untranslated regions. Ectopic miR-24 overexp  ...[more]

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