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PLoS One. 2008 Mar 26;3(3):e1864. doi: 10.1371/journal.pone.0001864.

p16(INK4a) translation suppressed by miR-24.

Author information

1
Laboratory of Cellular and Molecular Biology, National Institute on Aging-IRP, National Institutes of Health, Baltimore, Maryland, United States of America. alal@cbrinstitute.org

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.

PMID:
18365017
PMCID:
PMC2274865
DOI:
10.1371/journal.pone.0001864
[Indexed for MEDLINE]
Free PMC Article

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