<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Mubaid S</submitter><funding>NHGRI NIH HHS</funding><funding>Prostate Cancer Canada</funding><funding>Gouvernement du Canada | Canadian Institutes of Health Research</funding><funding>CIHR</funding><pagination>17261-17270</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6717253</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>116(35)</volume><pubmed_abstract>Debilitating cancer-induced muscle wasting, a syndrome known as cachexia, is lethal. Here we report a posttranscriptional pathway involving the RNA-binding protein HuR as a key player in the onset of this syndrome. Under these conditions, HuR switches its function from a promoter of muscle fiber formation to become an inducer of muscle loss. HuR binds to the &lt;i>STAT3&lt;/i> (&lt;i>signal transducer and activator of transcription 3&lt;/i>) mRNA, which encodes one of the main effectors of this condition, promoting its expression both in vitro and in vivo. While HuR does not affect the stability and the cellular movement of this transcript, HuR promotes the translation of the &lt;i>STAT3&lt;/i> mRNA by preventing miR-330 (microRNA 330)-mediated translation inhibition. To achieve this effect, HuR directly bi</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>HuR counteracts miR-330 to promote STAT3 translation during inflammation-induced muscle wasting.</pubmed_title><pmcid>PMC6717253</pmcid><funding_grant_id>D2014-14</funding_grant_id><funding_grant_id>R21 HG003679</funding_grant_id><funding_grant_id>FRN53888</funding_grant_id><funding_grant_id>U01 HG004571</funding_grant_id><funding_grant_id>MOP-142399</funding_grant_id><pubmed_authors>Ma JF</pubmed_authors><pubmed_authors>Mubaid S</pubmed_authors><pubmed_authors>Ashour K</pubmed_authors><pubmed_authors>Lian XJ</pubmed_authors><pubmed_authors>Cammas A</pubmed_authors><pubmed_authors>Sanchez BJ</pubmed_authors><pubmed_authors>Chittur SV</pubmed_authors><pubmed_authors>Robinson S</pubmed_authors><pubmed_authors>Gallouzi IE</pubmed_authors><pubmed_authors>Tenenbaum SA</pubmed_authors><pubmed_authors>Omer A</pubmed_authors><pubmed_authors>Di Marco S</pubmed_authors><pubmed_authors>Dormoy-Raclet V</pubmed_authors></additional><is_claimable>false</is_claimable><name>HuR counteracts miR-330 to promote STAT3 translation during inflammation-induced muscle wasting.</name><description>Debilitating cancer-induced muscle wasting, a syndrome known as cachexia, is lethal. Here we report a posttranscriptional pathway involving the RNA-binding protein HuR as a key player in the onset of this syndrome. Under these conditions, HuR switches its function from a promoter of muscle fiber formation to become an inducer of muscle loss. HuR binds to the &lt;i>STAT3&lt;/i> (&lt;i>signal transducer and activator of transcription 3&lt;/i>) mRNA, which encodes one of the main effectors of this condition, promoting its expression both in vitro and in vivo. While HuR does not affect the stability and the cellular movement of this transcript, HuR promotes the translation of the &lt;i>STAT3&lt;/i> mRNA by preventing miR-330 (microRNA 330)-mediated translation inhibition. To achieve this effect, HuR directly bi</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Aug</publication><modification>2025-04-04T20:10:24.378Z</modification><creation>2025-04-04T20:10:24.378Z</creation></dates><accession>S-EPMC6717253</accession><cross_references><pubmed>31405989</pubmed><doi>10.1073/pnas.1905172116</doi></cross_references></HashMap>