Reprogramming of Lipid Metabolism in Lung Cancer: An Overview with Focus on EGFR-Mutated Non-Small Cell Lung Cancer

Abstract

Lung cancer is the leading cause of cancer deaths worldwide. Most of lung cancer cases are classified as non-small cell lung cancers (NSCLC). EGFR has become an important therapeutic target for the treatment of NSCLC patients, and inhibitors targeting the kinase domain of EGFR are currently used in clinical settings. Recently, an increasing interest has emerged toward understanding the mechanisms and biological consequences associated with lipid reprogramming in cancer. Increased uptake, synthesis, oxidation, or storage of lipids has been demonstrated to contribute to the growth of many types of cancer, including lung cancer. In this review, we provide an overview of metabolism in cancer and then explore in more detail the role of lipid metabolic reprogramming in lung cancer development and progression and in resistance to therapies, emphasizing its connection with EGFR signaling. In addition, we summarize the potential therapeutic approaches targeting lipid metabolism for lung cancer treatment.

Identify metabolism-related genes IDO1, ALDH2, NCOA2, SLC7A5, SLC3A2, LDHB, and HPRT1 as potential prognostic markers and correlate with immune infiltrates in head and neck squamous cell carcinoma

“…Recent studies have shown that abnormal metabolite or intermediate metabolism in cancer may regulate immune cell proliferation, differentiation, activation, and function ( 12 , 13 ). Metabolic reprogramming has been studied in a range of tumors, including lung cancer ( 14 ), liver cancer ( 15 ), and glioma ( 16 ). However, metabolic reprogramming and immune response in HSCC have not been researched.…”

Reovirus uses temporospatial compartmentalization to orchestrate core versus outercapsid assembly

“…But reovirus is also undergoing clinical testing as a candidate cancer therapeutic since it replicates efficiently in cancer cells. In general, untransformed cells preferentially obtain fatty acids from extracellular sources, while metabolic changes in cancer cells often support enhanced de novo fatty acid synthesis and LD formation [ 66 , 67 ]. While major determinants of enteric and tumor specificity have been described [ 3 , 20 , 21 , 68 – 70 ], could additional host factors, such as LD abundance, also contribute to how well reovirus thrives in these environments?…”

Reovirus uses temporospatial compartmentalization to orchestrate core versus outercapsid assembly

“…But reovirus is also undergoing clinical testing as a candidate cancer therapeutic since it replicates efficiently in cancer cells. In general, untransformed cells preferentially obtain fatty acids from extracellular sources, while metabolic changes in cancer cells often support enhanced de novo fatty acid synthesis and LD formation 64,65 . While major determinants of enteric and tumor specificity have been described [19][20][21][66][67][68] , could additional host factors, such as LD abundance, also contribute to how well reovirus thrives in these environments?…”