Tumor metabolic reprogramming in lung cancer progression

Abstract

Metabolic reprogramming is an important characteristic of tumor cells. Tumor cells reprogram their metabolic pathways to meet the material, energy and redox force needs for rapid proliferation. Metabolic reprogramming changes the level or type of specific metabolites inside and outside cells, and promotes tumor growth by affecting gene expression, cell state and the tumor microenvironment. Glucose metabolism, glutamine metabolism and lipid metabolism are significant metabolic pathways in tumors. Targeting metabolic reprogramming can significantly inhibit tumor growth and induce apoptosis. Metabolic reprogramming also plays an important role in maintaining the growth advantage of tumor cells and enhancing the chemotherapy tolerance of lung cancer. This review summarizes abnormal changes in the metabolism of glucose, fat and amino acids in lung cancer, and the underlying molecular mechanism, with the aim of providing novel ideas for the prevention, early diagnosis and treatment of lung cancer.

Keywords: lung cancer; metabolic reprogramming.

Figure 1.

Tumor metabolism in lung cancer. An overview of key metabolic pathways and their associated crucial molecules in lung cancer cells is presented. Red arrows represent upregulated genes or metabolites involved in tumor metabolism, and the developed inhibitors are indicated. GLUT1, glucose transporter 1; HK2, hexokinase 2; G6P, glucose-6-phosphate; PFK1, phosphofructokinase 1; PEP, phosphoenolpyruvic acid; PKM2, pyruvate kinase M2; MCT, monocarboxylate transporter; LDH, lactate dehydrogenase; FA, fatty acid; FASN, fatty acid synthase; ACC, acetyl-CoA carboxylase; ACLY, ATP-citrate lyase; GAC, glutaminase C; ASCT2, alanine-serine-cysteine transporter 2; ATB0+, amino acid transporter B^0,+; LAT1, Human L-type amino acid transporter 1; α-KG, α-ketoglutarate; OAA, oxaloacetate; PDH, pyruvate dehydrogenase; GLS, glutaminase; KGA, kidney-type glutaminase.