p16(INK4a) translation suppressed by miR-24.

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 decre...

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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
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author 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
author_facet 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
author_sort Ashish Lal
collection DOAJ
description 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.
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spelling doaj.art-141f3df44cd24439bdc4dd836d1595e12022-12-22T02:26:21ZengPublic Library of Science (PLoS)PLoS ONE1932-62032008-03-0133e186410.1371/journal.pone.0001864p16(INK4a) translation suppressed by miR-24.Ashish LalHyeon Ho KimKotb AbdelmohsenYuki KuwanoRudolf PullmannSubramanya SrikantanRamesh SubrahmanyamJennifer L MartindaleXiaoling YangFariyal AhmedFrancisco NavarroDerek DykxhoornJudy LiebermanMyriam GorospeExpression 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.http://europepmc.org/articles/PMC2274865?pdf=render
spellingShingle 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
p16(INK4a) translation suppressed by miR-24.
PLoS ONE
title p16(INK4a) translation suppressed by miR-24.
title_full p16(INK4a) translation suppressed by miR-24.
title_fullStr p16(INK4a) translation suppressed by miR-24.
title_full_unstemmed p16(INK4a) translation suppressed by miR-24.
title_short p16(INK4a) translation suppressed by miR-24.
title_sort p16 ink4a translation suppressed by mir 24
url http://europepmc.org/articles/PMC2274865?pdf=render
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