{"title":"Acyl-CoA dehydrogenase long chain acts as a tumor-suppressive factor in lung adenocarcinoma progression.","authors":"Tingju Wei, Guowei Fu, Junjie Zhao, Fengan Cao, Danfeng Guo","doi":"10.1080/19336918.2025.2495676","DOIUrl":null,"url":null,"abstract":"<p><p>This study investigated the role of long-chain acyl-CoA dehydrogenase (ACADL) in lung adenocarcinoma (LUAD). ACADL was significantly downregulated in human LUAD tissues compared to normal lung tissues. In vitro, ectopic expression of ACADL in murine LLC cells decreased cell viability, migration, and invasion, while ACADL knockdown exhibited the opposite effect. <i>In vivo</i>, ACADL overexpression impeded tumor growth and metastasis. Mechanistically, ACADL hindered tumor progression by inducing cell cycle arrest, promoting apoptosis, and suppressing the epithelial-mesenchymal transition (EMT) process. These findings suggest ACADL acts as a tumor suppressor in LUAD progression.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2495676"},"PeriodicalIF":3.3000,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12026206/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Adhesion & Migration","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/19336918.2025.2495676","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/22 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
This study investigated the role of long-chain acyl-CoA dehydrogenase (ACADL) in lung adenocarcinoma (LUAD). ACADL was significantly downregulated in human LUAD tissues compared to normal lung tissues. In vitro, ectopic expression of ACADL in murine LLC cells decreased cell viability, migration, and invasion, while ACADL knockdown exhibited the opposite effect. In vivo, ACADL overexpression impeded tumor growth and metastasis. Mechanistically, ACADL hindered tumor progression by inducing cell cycle arrest, promoting apoptosis, and suppressing the epithelial-mesenchymal transition (EMT) process. These findings suggest ACADL acts as a tumor suppressor in LUAD progression.
期刊介绍:
Cell Adhesion & Migration is a multi-disciplinary, peer reviewed open access journal that focuses on the biological or pathological implications of cell-cell and cell-microenvironment interactions. The main focus of this journal is fundamental science. The journal strives to serve a broad readership by regularly publishing review articles covering specific disciplines within the field, and by publishing focused issues that provide an overview on specific topics of interest within the field.
Cell Adhesion & Migration publishes relevant and timely original research, as well as authoritative overviews, commentaries, and perspectives, providing context for the work presented in Cell Adhesion & Migration and for key results published elsewhere. Original research papers may cover all topics important in the field of cell-cell and cell-matrix interactions. Cell Adhesion & Migration also publishes articles related to cell biomechanics, biomaterial, and development of related imaging technologies.