Alternative Energy: Breaking Down the Diverse Metabolic Features of Lung Cancers

Abstract

Metabolic reprogramming is a hallmark of cancer initiation, progression, and relapse. From the initial observation that cancer cells preferentially ferment glucose to lactate, termed the Warburg effect, to emerging evidence indicating that metabolic heterogeneity and mitochondrial metabolism are also important for tumor growth, the complex mechanisms driving cancer metabolism remain vastly unknown. These unique shifts in metabolism must be further investigated in order to identify unique therapeutic targets for individuals afflicted by this aggressive disease. Although novel therapies have been developed to target metabolic vulnerabilities in a variety of cancer models, only limited efficacy has been achieved. In particular, lung cancer metabolism has remained relatively understudied and underutilized for the advancement of therapeutic strategies, however recent evidence suggests that lung cancers have unique metabolic preferences of their own. This review aims to provide an overview of essential metabolic mechanisms and potential therapeutic agents in order to increase evidence of targeted metabolic inhibition for the treatment of lung cancer, where novel therapeutics are desperately needed.

Comprehensive Analysis of Subtypes and Identification of Key lncRNAs Based on Glutamine Metabolism-Related Long Noncoding RNAs

“…We identified 11 commonly shared glutamine metabolismrelated lncRNAs in three different LUAD data cohorts using glutamine metabolism scores and ssGSEA. Several previous studies have highlighted the metabolic heterogeneity in lung tumors [30], suggesting that LUAD may have different metabolic phenotypes. To investigate the metabolic phenotypes, we classified the LUAD samples into three glutamine metabolic subtypes based on the 11 glutamine metabolismassociated lncRNAs.…”

The sodium/myo-inositol co-transporter SLC5A3 promotes non-small cell lung cancer cell growth

“…Metabolic reprogramming is a key hallmark of NSCLC and is critical for the sustained cancer cell proliferation [35][36][37]. Like other malignancies, altered metabolic features in NSCLC can provide enough nutrients for cancer growth [35][36][37].…”

“…Metabolic reprogramming is a key hallmark of NSCLC and is critical for the sustained cancer cell proliferation [35][36][37]. Like other malignancies, altered metabolic features in NSCLC can provide enough nutrients for cancer growth [35][36][37]. Ji et al, have demonstrated that SLC7A11 is a key regulator of metabolic reprogramming during NSCLC tumorigenesis and progression and is essential for glucose metabolism, glutamine dependency, and intracellular GSH/GSSG redox balance in NSCLC cells [38].…”

Unraveling the Rewired Metabolism in Lung Cancer Using Quantitative NMR Metabolomics

“…The increased dependence of lung cancer cells on glucose uptake and upregulated glycolysis provides an interesting biochemical basis for developing systemic anticancer treatments that preferentially target cancer cells by pharmacological inhibition of glycolysis. Glucose transporters and glycolytic enzymes are overexpressed in lung cancer, and inhibition of these targets provides an attractive avenue for developing new anticancer treatments [ 85 ]. Several inhibitors of glycolytic enzymes and transporters are in preclinical development, yet none of them have approved status [ 4 ].…”