Abstract

Normal cells typically use mitochondrial oxidative phosphorylation to metabolize glucose and switch over to glycolysis only in hypoxic or anoxic environment. However, cancer cells avidly consume glucose for energy by glycolysis to survive in the hypoxic environment of malignant lesions, a phenomenon known as the Warburg effect, the glycolytic phenotype offers growth advantages to cancer cells by resisting apoptosis. This unique metabolic characteristic of cancer cells has identified the mitochondrion as a target for cancer therapy.In vitro, different cancer cells were treated with DCA-Na, all cancer cell lines were affected by the treatment with DCA-Na, the B16F10 cell line was the most sensitive to the treatment, decreased the cellular viability, induced cellular death by apoptosis, affecting different metabolic pathways (LDH, PKA/cAMP, HIF-1α, and GAPDH), decreased the capacity of cellular invasion and angiogenesis. In vivo the DCA-Na treatment induced 20% survival and decreased the tumoral diameter, volume and weight, without affect the body weight and avoid metastasis in C57BL/6 mice. Our results suggest that DCA-Na is a good candidate as a new agent in the treatment of cancer due to its antitumoral properties in vitro and in vivo.

Key words: Cancer, sodium dichloroacetate, glycolysis, melanoma.