<HashMap><database>biostudies-literature</database><scores/><additional><submitter>La Montagna M</submitter><funding>Cancer Research UK</funding><pagination>2673-2689</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8408205</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>28(9)</volume><pubmed_abstract>AMP-activated protein kinase (AMPK) is a critical sensor of energy status that coordinates cell growth with energy balance. In non-small cell lung cancer (NSCLC) the role of AMPKα is controversial and its contribution to lung carcinogenesis is not well-defined. Furthermore, it remains largely unknown whether long non-coding RNAs (lncRNAs) are involved in the regulation of AMPK-mediated pathways. Here, we found that loss of AMPKα in combination with activation of mutant KRAS&lt;sup>G12D&lt;/sup> increased lung tumour burden and reduced survival in Kras&lt;sup>LSLG12D/+&lt;/sup>/AMPKα&lt;sup>fl/fl&lt;/sup> mice. In agreement, functional in vitro studies revealed that AMPKα silencing increased growth and migration of NSCLC cells. In addition, we identified an AMPKα-modulated lncRNA, KIMAT1 (ENSG00000228709), w</pubmed_abstract><journal>Cell death and differentiation</journal><pubmed_title>AMPKα loss promotes KRAS-mediated lung tumorigenesis.</pubmed_title><pmcid>PMC8408205</pmcid><funding_grant_id>C5759/A20971</funding_grant_id><pubmed_authors>La Montagna M</pubmed_authors><pubmed_authors>Shi L</pubmed_authors><pubmed_authors>Magee P</pubmed_authors><pubmed_authors>Sahoo S</pubmed_authors><pubmed_authors>Fassan M</pubmed_authors><pubmed_authors>Garofalo M</pubmed_authors></additional><is_claimable>false</is_claimable><name>AMPKα loss promotes KRAS-mediated lung tumorigenesis.</name><description>AMP-activated protein kinase (AMPK) is a critical sensor of energy status that coordinates cell growth with energy balance. In non-small cell lung cancer (NSCLC) the role of AMPKα is controversial and its contribution to lung carcinogenesis is not well-defined. Furthermore, it remains largely unknown whether long non-coding RNAs (lncRNAs) are involved in the regulation of AMPK-mediated pathways. Here, we found that loss of AMPKα in combination with activation of mutant KRAS&lt;sup>G12D&lt;/sup> increased lung tumour burden and reduced survival in Kras&lt;sup>LSLG12D/+&lt;/sup>/AMPKα&lt;sup>fl/fl&lt;/sup> mice. In agreement, functional in vitro studies revealed that AMPKα silencing increased growth and migration of NSCLC cells. In addition, we identified an AMPKα-modulated lncRNA, KIMAT1 (ENSG00000228709), w</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Sep</publication><modification>2025-04-18T22:27:08.658Z</modification><creation>2025-04-07T10:13:21.652Z</creation></dates><accession>S-EPMC8408205</accession><cross_references><pubmed>34040167</pubmed><doi>10.1038/s41418-021-00777-0</doi></cross_references></HashMap>