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p16INK4a Translation Suppressed by miR-24

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83742 journal.pone.0001864.pdf (915.13 KB)

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2008

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10.1371/journal.pone.0001864

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Public Library of Science
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Lal, Ashish, Hyeon Ho Kim, Kotb Abdelmohsen, Yuki Kuwano, Rudolf Pullmann, Subramanya Srikantan, Ramesh Subrahmanyam, et al. 2008. “p16INK4a Translation Suppressed by miR-24.” Edited by Thomas Preiss. PLoS ONE 3 (3): e1864. https://doi.org/10.1371/journal.pone.0001864.

Abstract

Background: Expression of the tumor suppressor p16(INK4a) increases during aging and replicative senescence.Methodology/Principal Findings: 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. Conclusions: /Significance: Together, our results suggest that miR-24 represses the initiation and elongation phases of p16 translation.

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http://nrs.harvard.edu/urn-3:HUL.InstRepos:41483413

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