<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Huna A</submitter><funding>Institut National Du Cancer</funding><pagination>318</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10680185</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>42(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>TGFβ induces several cell phenotypes including senescence, a stable cell cycle arrest accompanied by a secretory program, and epithelial-mesenchymal transition (EMT) in normal epithelial cells. During carcinogenesis cells lose the ability to undergo senescence in response to TGFβ but they maintain an EMT, which can contribute to tumor progression. Our aim was to identify mechanisms promoting TGFβ-induced senescence escape.&lt;h4>Methods&lt;/h4>In vitro experiments were performed with primary human mammary epithelial cells (HMEC) immortalized by hTert. For kinase library screen and modulation of gene expression retroviral transduction was used. To characterize gene expression, RNA microarray with GSEA analysis and RT-qPCR were used. For protein level and localization, Western b</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>RSK3 switches cell fate: from stress-induced senescence to malignant progression.</pubmed_title><pmcid>PMC10680185</pmcid><funding_grant_id>PLBio 18-144</funding_grant_id><funding_grant_id>PLBio 15-013</funding_grant_id><pubmed_authors>Huna A</pubmed_authors><pubmed_authors>Coute Y</pubmed_authors><pubmed_authors>Defossez PA</pubmed_authors><pubmed_authors>Boissan M</pubmed_authors><pubmed_authors>Pakulska V</pubmed_authors><pubmed_authors>Makulyte G</pubmed_authors><pubmed_authors>Saintigny P</pubmed_authors><pubmed_authors>Ruisseaux C</pubmed_authors><pubmed_authors>Zhu K</pubmed_authors><pubmed_authors>Martin N</pubmed_authors><pubmed_authors>Bernard D</pubmed_authors><pubmed_authors>Hernandez-Vargas H</pubmed_authors><pubmed_authors>Lodillinsky C</pubmed_authors><pubmed_authors>Flaman JM</pubmed_authors></additional><is_claimable>false</is_claimable><name>RSK3 switches cell fate: from stress-induced senescence to malignant progression.</name><description>&lt;h4>Background&lt;/h4>TGFβ induces several cell phenotypes including senescence, a stable cell cycle arrest accompanied by a secretory program, and epithelial-mesenchymal transition (EMT) in normal epithelial cells. During carcinogenesis cells lose the ability to undergo senescence in response to TGFβ but they maintain an EMT, which can contribute to tumor progression. Our aim was to identify mechanisms promoting TGFβ-induced senescence escape.&lt;h4>Methods&lt;/h4>In vitro experiments were performed with primary human mammary epithelial cells (HMEC) immortalized by hTert. For kinase library screen and modulation of gene expression retroviral transduction was used. To characterize gene expression, RNA microarray with GSEA analysis and RT-qPCR were used. For protein level and localization, Western b</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Nov</publication><modification>2026-05-28T20:39:27.143Z</modification><creation>2025-02-18T23:29:38.714Z</creation></dates><accession>S-EPMC10680185</accession><cross_references><pubmed>38008756</pubmed><doi>10.1186/s13046-023-02909-5</doi></cross_references></HashMap>