{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Vitos-Faleato J"],"funding":["European Research Council"],"pagination":["2588-2596"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7007552"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["117(5)"],"pubmed_abstract":["Malignant transformation entails important changes in the control of cell proliferation through the rewiring of selected signaling pathways. Cancer cells then become very dependent on the proper function of those pathways, and their inhibition offers therapeutic opportunities. Here we identify the stress kinase p38α as a nononcogenic signaling molecule that enables the progression of KrasG12V-driven lung cancer. We demonstrate in vivo that, despite acting as a tumor suppressor in healthy alveolar progenitor cells, p38α contributes to the proliferation and malignization of lung cancer epithelial cells. We show that high expression levels of p38α correlate with poor survival in lung adenocarcinoma patients, and that genetic or chemical inhibition of p38α halts tumor growth in lung cancer mou"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Requirement for epithelial p38α in KRAS-driven lung tumor progression."],"pmcid":["PMC7007552"],"funding_grant_id":["294665"],"pubmed_authors":["Vitos-Faleato J","Gutierrez-Prat N","Nebreda AR","Llonch E","Barbacid M","Real SM","Villanueva A","Drosten M"],"additional_accession":[]},"is_claimable":false,"name":"Requirement for epithelial p38α in KRAS-driven lung tumor progression.","description":"Malignant transformation entails important changes in the control of cell proliferation through the rewiring of selected signaling pathways. Cancer cells then become very dependent on the proper function of those pathways, and their inhibition offers therapeutic opportunities. Here we identify the stress kinase p38α as a nononcogenic signaling molecule that enables the progression of KrasG12V-driven lung cancer. We demonstrate in vivo that, despite acting as a tumor suppressor in healthy alveolar progenitor cells, p38α contributes to the proliferation and malignization of lung cancer epithelial cells. We show that high expression levels of p38α correlate with poor survival in lung adenocarcinoma patients, and that genetic or chemical inhibition of p38α halts tumor growth in lung cancer mou","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Feb","modification":"2025-04-22T19:29:01.267Z","creation":"2025-04-06T02:48:07.018Z"},"accession":"S-EPMC7007552","cross_references":{"pubmed":["31969449"],"doi":["10.1073/pnas.1921404117"]}}