Pathophysiological mechanisms of death resistance in colorectal carcinoma

Table 3 Glucose-dependent mechanisms in death resistance of colon cancer

Classification	Molecule	Expression and mechanism	Ref.
Glucose uptake
Transporters	GLUT1	Abnormal expression of GLUT1 in colon cancer	[128,129]
		Hypoxia-induced expression of GLUT1 by HIF-1 binding to the GLUT1 promoter	[96,131,132]
		GLUT1-mediated glucose uptake promoted drug resistance in colon cancer cells	[136]
	GLUT3,4	Abnormal expression of GLUT3,4 in colon cancer	[19,27,130]
	SGLT1	Abnormal expression of SGLT1 in colon cancer	[27,115]
		Stabilization of membrane SGLT1 expression is dependent on EGFR in a kinase-independent mechanism	[117,134]
Glucose metabolism
Enzymes	PK	Upregulation of PKM2 isoform in chemoresistant cancer cells	[132]
	PDK-1	PDK-1 as a novel Wnt target gene improved colon cancer cell survival via enhancement of glycolysis	[142]
	PDK-3	HIF1-mediated upregulation of PDK-3 inhibited mitochondrial phosphorylation and promoted drug resistance	[143]
	HK, GAPDH	HIF1-dependent transcriptional upregulation	[45,96]
	PDH	Decreased expression in colon cancer cells	[141]
Carriers	MPC	Reduction of MPC activity promoted glycolysis and maintenance of stemness properties	[144]
Products	ATP	Elevation of intracellular ATP promoted cancer cell survival and induced drug resistance	[145,146]
	Pyruvate	Pyruvate prevented hypoxia-induced necroptosis through suppression of mitochondrial free radicals in an ATP-independent mechanism	[19]

GLUT: Glucose transporter; SGLT1: Sodium-dependent glucose transporter 1; EGFR: Epidermal growth factor receptor; PK: Pyruvate kinase; PDK: Pyruvate dehydrogenase kinase; HK: Hexokinase; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; PK: Pyruvate kinase; PDH: Pyruvate dehydrogenase; MPC: Mitochondrial pyruvate carrier.