Lung adenocarcinoma (LUAD) remains the most common subtype of non–small cell lung cancer with poor survival. Dysregulation of mitochondrial energy metabolism (MEM) can be considered as major driver for LUAD pathogenesis among Chronic obstructive pulmonary disease (COPD) patients. Hence, deeper understanding of MEM carcinogenic role for LUAD patients can provide novel insights into LUAD pathogenesis for COPD patients. By employing integrative bioinformatic approaches, such as Limma and WGCNA in LUAD bulk profile (GSE32863), we first identified COPD and MEM (CM)-associated DEGs for LUAD patients, and these DEGs can divide LUAD patients from TCGA-LUAD cohort into 2 risk groups. Next, Lasso-cox regression and multi-variate cox regression identified CM-associated predictive model and hub gene for LUAD patients both in TCGA-LUAD cohort and GSE13213. Indeed, hub gene molecular and immune characters were estimated at LUAD bulk level (TCGA-LUAD cohort) and single-cell level (GSE203360). Besides, drug sensitivity and molecular docking analysis confirmed potential therapeutic agent targeting hub gene for the treatment of LUAD. 8 CM-associated gene signatures can divide LUAD patients into 2 molecular subgroups and guide the prognostic model construction for LUAD patients. TPI1 can be considered as CM-associated hub gene involved in LUAD progression. 17-AAG can be considered as drug reproposing framework for the treatment of LUAD. This study first highlighted the predictive and therapeutic potentials of CM, and highlighted TPI1 pathogenic role for LUAD patients.
Wang et al. (Sun,) studied this question.