Fig. 4
From: Molecular mechanisms of tumor resistance to radiotherapy
The relationship between metabolic reprogramming and radioresistance. Active glycolysis and lipid metabolism, which are typical of cancer metabolism, promote the development of radioresistance by mediating the development of immunosuppressive microenvironments and blocking apoptosis. In addition, the high expression of glutamine synthetase, purines, and serine protease inhibitor E2 can promote DNA damage repair, thereby leading to radioresistance. FAO: fatty acid oxidation, FFA: free fatty acid, Glu; glucose, G6P: glucose-6-phosphate, G3P: glyceraldehyde triphosphate, DHAP: dihydroxyacetone phosphate, FBP: fructose-1,6-bisphosphate, GS: glutamine synthetase, ATM: ataxia-telangiectasia mutated, NF-κB: nuclear factor-kappa B, Cyt c: cytochrome c, HK2: hexokinase 2, PFK1: phosphofructokinase 1, MDSCs: myeloid-derived suppressor cells, DHAP: dihydroxyacetone phosphate, HIF-1α: hypoxia-inducible factor 1α, SERPINE2: serine protease inhibitor E2, TCA cycle: tricarboxylic acid cycle