Fig. 1

Key signalling pathways supporting glycolysis in tumor cells. A Hypoxia and HIF1α signalling dominates glycolysis in tumor cells via regulating multiple signalling pathways involved in both glycolytic and OXPHOS metabolisms. HIF-1 promotes glycolysis through increasing glucose influx and upregulating the expression of glycolytic enzymes. Meanwhile, it suppresses OXPHOS via disrupting mitochondrial functions and biogenesis. B The famous carcinogenic RTK-PI3K–AKT–mTORC1 signalling pathway interplays with HIF-1 to promote glycolytic metabolism. C Oncogenic mutation such as KRAS stimulates glucose uptake and facilitates glycolytic activities. Glucose-6P glucose-6-phosphate; Fructose-6P fructose-6-phosphate; Fructose-1,6-biP fructose 1,6- bis phosphatase; DHAP dihydroxyacetone phosphate; GA3P glyceraldehyde 3-phosphate; NAD+  nicotinamide adenine dinucleotide; NADH nicotinamide adenine dinucleotide (NAD)+ hydrogen (H); 3PG 3-phosphoglycerate; 2PG 2-phosphoglycerate; PEP phosphoenolpyruvate; MPC mitochondrial pyruvate carrier; Acetyl-CoA Acetyl-coenzyme A; OAA oxaloacetate; SucCoA succinyl-coenzyme A; α-KG alpha-ketoglutarate; ETC electron transport chain; c-Myc cellular myelocytomatosis ongogene; MCT monocarboxylate transporters. Image was created with www.BioRender.com