Background: Expression of the tumor suppressor p16INK4a 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.
CITATION STYLE
Lal, A., Kim, H. H., Abdelmohsen, K., Kuwano, Y., Pullmann, R., Srikantan, S., … Gorospe, M. (2008). p16INK4a translation suppressed by miR-24. PLoS ONE, 3(3). https://doi.org/10.1371/journal.pone.0001864
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