Table 1. Role of key multifaceted regulators in cancer glucose metabolism.

Metabolism procedures	Key molecules	Potential targets	Biological effects	Refs
Glycolysis process	p53	GLUT1 and GLUT4	Prevent the glucose uptake	[32]
	HIF-1	GLUT1 and GLUT3	Promote the glucose entry into the tumor cells	[48]
	HIF-1	HK2	Enhance the phosphorylation of glucose	[49]
	HIF-1	LDHA and MCT4	Facilitate the conversion of pyruvate to lactate and the removal of lactate from tumor cells	[51]
	TIGAR	Fructose-2, 6-bisphosphate	Decrease the glycolytic rate	[63]
	TIGAR	NADPH	Lower the intracellular ROS level	[67]
	miR-143	HK2	Reduce glucose metabolism and inhibit tumor cell proliferation	[79]
	miR-155	STAT3 and C/EBPβ	Control the aerobic glycolysis of tumor cells	[81]
	miR-195-5p	GLUT3	Suppress the glucose uptake, inhibit tumor cell growth and promote apoptosis of tumor cells	[82]
Oxidative phosphorylation process	p53	SCO2 and GLS2	Increase the use of TCA cycle and up-regulate the rate of oxidative phosphorylation	[34, 35]
	HIF-1	PDK1, MXI1 and COX4	Repress mitochondrial activities and decrease oxygen consumption in hypoxia	[52]
	miR-141, miR-200a	p38α	Control tumor oxidative stress response and regulate redox potential	[83]

Abbreviation: GLUT1: Glucose transporter 1; SCO2: Synthesis of cytochrome c oxidase 2; GLS2: Glutaminase 2; TCA cycle: Tricarboxylic acid cycle; HIF-1: Hypoxia-inducible factor 1; HK2: Hexokinase 2; LDHA: Lactate dehydrogenase A; MCT4: Monocarboxylate transporter 4; PDK1: Pyruvate dehydrogenase kinase 1; MXI1: Max interactor 1; COX4: Cytochrome c oxidase subunit 4.