Authors
Xinyi Qian, Juze Yang, Jiayi Ren, Xiaowei Mao, Jia Li, Tengfei Sun, Liangliang Dong, Enguo Chen, Yan Lu, Pengyuan Liu
Published in
Advanced science (Weinheim, Baden-Wurttemberg, Germany). Pages e77950. Sep 27, 2026. Epub Sep 27, 2026.
Abstract
Lung cancer remains the leading cause of cancer-related mortality, with extremely high energy demands during progression. Long non-coding 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, GSLR, as a driver of lung adenocarcinoma (LUAD) progression. GSLR is markedly upregulated in LUAD, and its high expression is associated with poor patient prognosis. Nutrient restriction reduces chromatin accessibility at the GSLR locus via altered histone marks, whereas CTCF activates its transcription. Mechanistically, GSLR directly binds the RNA helicase DHX9 and recruits it to the creatine kinase B (CKB) promoter, arresting R-loop 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 GSLR as a novel regulator of energy homeostasis that promotes lung cancer progression through the GSLR/DHX9/CKB axis. Targeting GSLR may thus represent a promising therapeutic strategy for LUAD.
PMID:
42801620
Bibliographic data and abstract were imported from PubMed on 28 Sep 2026.
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