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Unrestrained glycolysis characterizes energy meta-bolism in cancer cells.Thus, antiglycolytic reagents such as 2-deoxy-D-glucose (2-DG) and 3-bromopyruvate(3-BrPA) may be used as anticancer drugs. In the present study, we examined theanticancer effects of 2-DG and 3-BrPA in pancreatic cancer cells and investigatedwhether these effects were regulated by hypoxia-inducible factor-1α (HIF-1α).To this end, 2-DG and 3-BrPA were administered to wild-type (wt) MiaPaCa2 andPanc-1 pancreatic cancer cells that were incubated under hypoxic (HIF-1α-positive)or normoxic (HIF-1α-negative) conditions. In addition, 2-DG and 3-BrPA were alsoadministered to si-MiaPaCa2 and si-Panc-1 cells that lacked HIF-1α as a resultof RNA interference. Following drug exposure, cell population was measured usinga viability assay. Both HIF-1α-positive and HIF-1α-negative MiaPaCa2 cells werefurther studied for their expression of Cu/Zn-superoxide dismutase (SOD1) andpoly(ADP-ribose) polymerase (PARP) and for their contents of ATP and fumarate.In the viability assay, either 2-DG or 3-BrPA decreased the tested cells. Concurrentuse of 2-DG and 3-BrPA resulted in a greater decrease of cells and also facilitatedATP depletion. In addition, 3-BrPA was seen to both decrease SOD1 and increasefumarate, which suggests that the reagent impaired the mitochondria. 3-BrPA alsodecreased both full-length PARP and cleaved PARP, which suggests that 3-BrPA-induceddecrease in cell population was a result of cell necrosis rather than apoptosis.When HIF-1α was induced in wt-MiaPaCa2 cells by hypoxia, some effects of 2-DGand 3-BrPA were attenuated. We conclude that: i) concurrent use of 2-DG and 3-BrPAhas better anticancer effects in pancreatic cancer cells, ii) 3-BrPA impairs themitochondria of pancreatic cancer cells and induces cell necrosis, and iii) HIF-1αregulates the anticancer effects of 2-DG and 3-BrPA in pancreatic cancer cells.

Separate and concurrent use of 2-deoxy-D-glucose and 3-bromopyruvate in pancreatic cancer cells