p16(INK4a) translation suppressed by miR-24 |
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Authors: | Lal Ashish Kim Hyeon Ho Abdelmohsen Kotb Kuwano Yuki Pullmann Rudolf Srikantan Subramanya Subrahmanyam Ramesh Martindale Jennifer L Yang Xiaoling Ahmed Fariyal Navarro Francisco Dykxhoorn Derek Lieberman Judy Gorospe Myriam |
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Affiliation: | Laboratory of Cellular and Molecular Biology, National Institute on Aging-IRP, National Institutes of Health, Baltimore, Maryland, United States of America. alal@cbrinstitute.org |
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Abstract: | BackgroundExpression of the tumor suppressor p16INK4a increases during aging and replicative senescence.Methodology/Principal FindingsHere, 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.Conclusions/SignificanceTogether, our results suggest that miR-24 represses the initiation and elongation phases of p16 translation. |
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