Table 1.

Metabolic changes in different models of epithelial ovarian cancer.

Pathways	Models of Study in EOC	Description of Evidence	References
Glycolysis	Tissue	Increase in Pyruvate kinase M2 (PKM2), inducible Nitric Oxide Synthase (iNOS), and glycolytic genes (i.e., SLC2A1, SLC2A4, HK1, HK2, PFKFB3, PDK3, and LDHA). Glycolytic metabolism was observed to increase in EOC cells in comparison with non-cancer cells.	[36]
	Tissue	The glycolytic enzyme HK2 is higher in EOC tissues than in normal ovarian tissues, in advanced stages, and serous carcinomas than in non-serous carcinomas.	[37]
	Tissue and cell lines	The expression of glycolytic proteins is higher in HGSOC and advanced stages of OC (III / IV) than in the early stages. Glycolysis inhibitors decrease the proliferation of HGSOC cell lines sensitive and resistant to therapy.	[38]
OXPHOS	Tissue	Increase in mtDNA, numbers of mitochondria, and levels of proteins associated with OXPHOS (i.e., PGC-1α).	[41]
	Tissue	Increased OXPHOS is relative to non-cancer ovarian tissue.	[43]
	Tissue and cell lines	Increased levels of TRAP1 were associated with higher OXPHOS, stage, resistance to therapy, and lower survival.	[44]
	Tissue, cell lines, Patient-derived xenografts (PDX)	HGSOC high in OXPHOS displays a better prognosis and sensitivity to chemotherapy.	[45]