Lal, AshishKim, Hyeon HoAbdelmohsen, KotbKuwano, YukiPullmann, Rudolf Jr.Srikantan, SubramanyaSubrahmanyam, RameshMartindale, JenniferYang, XiaolingAhmed, FariyalNavarro, FranciscoDykxhoorn, DerekLieberman, JudyGorospe, Myriam2019-10-052008Lal, 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.0001864.1932-6203http://nrs.harvard.edu/urn-3:HUL.InstRepos:41483413Background: 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.en-USJournal Article2019-10-0510.1371/journal.pone.0001864