{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Korde A"],"funding":["U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)","NHLBI NIH HHS","U.S. Department of Defense (United States Department of Defense)"],"pagination":["511"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11953391"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(1)"],"pubmed_abstract":["Cigarette smoke (CS) creates a \"cancer field\" in the lung that promotes malignant transformation. The molecular changes within this field are not fully characterized. We examined the significance of microRNA-1 (miR-1) downregulation as one of these changes. We found that tumor miR-1 levels in three non-small cell lung cancer cohorts show inverse correlations with the smoking burden. Lung MiR-1 levels follow a spatial gradient, have prognostic significance, and correlate inversely with the molecular markers of injury. In CS-exposed lungs, miR-1 is specifically downregulated in the endothelium. Exposure to CS induces angiogenesis by selectively degrading mature miR-1 via a vascular endothelial growth factor-driven pathway. Applying a multi-step molecular screen, we identified angiogenic gene"],"journal":["Communications biology"],"pubmed_title":["Cigarette smoke induces angiogenic activation in the cancer field through dysregulation of an endothelial microRNA."],"pmcid":["PMC11953391"],"funding_grant_id":["R01 HL155948","R01CA225977","R00 HL098695","PR211314"],"pubmed_authors":["Diao L","Korde A","Zhang JG","Anderson S","Boffa DJ","Hu B","Wang J","Yan X","Moghaddam SJ","Velasco WV","Puchalski JT","Takyar SS","Ramaswamy A","Sauler M","Pisani MA","Jin L"],"additional_accession":[]},"is_claimable":false,"name":"Cigarette smoke induces angiogenic activation in the cancer field through dysregulation of an endothelial microRNA.","description":"Cigarette smoke (CS) creates a \"cancer field\" in the lung that promotes malignant transformation. The molecular changes within this field are not fully characterized. We examined the significance of microRNA-1 (miR-1) downregulation as one of these changes. We found that tumor miR-1 levels in three non-small cell lung cancer cohorts show inverse correlations with the smoking burden. Lung MiR-1 levels follow a spatial gradient, have prognostic significance, and correlate inversely with the molecular markers of injury. In CS-exposed lungs, miR-1 is specifically downregulated in the endothelium. Exposure to CS induces angiogenesis by selectively degrading mature miR-1 via a vascular endothelial growth factor-driven pathway. Applying a multi-step molecular screen, we identified angiogenic gene","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-06-02T20:38:20.311Z","creation":"2025-06-25T03:04:39.015Z"},"accession":"S-EPMC11953391","cross_references":{"pubmed":["40155749"],"doi":["10.1038/s42003-025-07710-y"]}}