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Long non\u2010coding RNAs (lncRNAs) have emerged as crucial regulators in cancer metabolism; however, their role in reprogramming energy metabolism in lung cancer remains incompletely understood. In this study, we identify a glucose\/glutamine sensitive lncRNA,\n                    <jats:italic>GSLR<\/jats:italic>\n                    , as a driver of lung adenocarcinoma (LUAD) progression.\n                    <jats:italic>GSLR<\/jats:italic>\n                    is markedly upregulated in LUAD, and its high expression is associated with poor patient prognosis. Nutrient restriction reduces chromatin accessibility at the\n                    <jats:italic>GSLR<\/jats:italic>\n                    locus via altered histone marks, whereas CTCF activates its transcription. Mechanistically,\n                    <jats:italic>GSLR<\/jats:italic>\n                    directly binds the RNA helicase DHX9 and recruits it to the creatine kinase B (CKB) promoter, arresting R\u2010loop accumulation and thereby promoting CKB transcription. Elevated CKB expression sustains intracellular ATP homeostasis, thereby stabilizing mitochondrial membrane potential, preventing calcium overload, and reducing reactive oxygen species (ROS) accumulation. Collectively, our findings identify\n                    <jats:italic>GSLR<\/jats:italic>\n                    as a novel regulator of energy homeostasis that promotes lung cancer progression through the\n                    <jats:italic>GSLR<\/jats:italic>\n                    \/DHX9\/CKB axis. Targeting\n                    <jats:italic>GSLR<\/jats:italic>\n                    may thus represent a promising therapeutic strategy for LUAD.\n                  <\/jats:p>","DOI":"10.1002\/advs.77950","type":"journal-article","created":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T18:00:31Z","timestamp":1790532031000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<i>GSLR<\/i>\n                    Drives Lung Adenocarcinoma as a Critical Regulator of Energy Homeostasis Through Creatine Kinase B Activation"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6108-3386","authenticated-orcid":false,"given":"Xinyi","family":"Qian","sequence":"first","affiliation":[{"name":"Department of Pulmonary and Critical Care Medicine Regional Medical Center For National Institute of Respiratory Diseases Sir Run Run Shaw Hospital and Institute of Translational Medicine Zhejiang University School of 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Cancer Metabolism Zhejiang University School of Medicine  Hangzhou Zhejiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8386-8416","authenticated-orcid":false,"given":"Pengyuan","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Pulmonary and Critical Care Medicine Regional Medical Center For National Institute of Respiratory Diseases Sir Run Run Shaw Hospital and Institute of Translational Medicine Zhejiang University School of Medicine  Hangzhou Zhejiang China"},{"name":"Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism Zhejiang University School of Medicine  Hangzhou Zhejiang 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