Glucose metabolic phenotype of pancreatic cancer

Table 2 Systematic review of the literature involving Krebs cycle enzymes and pancreatic ductal adenocarcinoma

Glycolytic Enzyme	In vitro/In vivo/clinical studies
	Ref.	Summary
Pyruvate dehydrogenase	[30,109,131,132,140,154,164,170,171,173,177,179,180,184-188]	Inhibition of pyruvate dehydrogenase kinase (the activity of which is regulated by pyruvate dehydrogenase) stimulates the Krebs cycle and reverses the Warburg effect.
Pyruvate carboxylase	[141]	Over expressed in human and murine PDAC
Citrate synthase	[67,124,179]	Over expressed in PDAC. Activity of citrate synthase also higher in PDAC compared to normal tissue
Aconitase	[67]	Mitochrondrial isoform under-expressed
Isocitrate dehydrogenase	[67,158,189,190]	Regulated by HuR (an RNA-binding protein) in PDAC.
a-ketoglutarate dehydrogenase	[67,187]	Marginally increased in murine PDAC
Succinyl-CoA synthetase	[67]	Reduced expression
Succinic dehydrogenase	[67,128]	Over expressed in human and murine PDAC
Fumarase	[30]	HIF-1α increases fumarate by inhibiting distal mitochondrial metabolisms
Malate dehydrogenase	[50,64,67]	Over expressed in human and murine PDAC. Possible candidate biomarker

HIF: Hypoxia-inducible factor; PDAC: Pancreatic ductal adenocarcinoma.