p16(INK4a) translation suppressed by miR-24.

• Main Authors: Ashish Lal, Hyeon Ho Kim, Kotb Abdelmohsen, Yuki Kuwano, Rudolf Pullmann, Subramanya Srikantan, Ramesh Subrahmanyam, Jennifer L Martindale, Xiaoling Yang, Fariyal Ahmed, Francisco Navarro, Derek Dykxhoorn, Judy Lieberman, Myriam Gorospe
• Format: Article
• Language: English
• Published: Public Library of Science (PLoS) 2008-03-01
• Series: PLoS ONE
• Online Access: http://europepmc.org/articles/PMC2274865?pdf=render

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.