期刊
CANCER LETTERS
卷 346, 期 2, 页码 300-308出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2014.01.015
关键词
Metformin; Dichloroacetate (DCA); Oxidative stress; Glucose deprivation; Glutathione contents
类别
资金
- National R&D Program for Cancer Control, Ministry for Health and Welfare, Republic of Korea [131280]
- Korea Health Promotion Institute [1320230-1] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
To investigate sensitization of metformin-cytotoxicity, cancer cells were treated with dichloroacetate COCA), an inhibitor of pyruvate dehydrogenase kinase (PDK). Metformin-cytotoxicity was mainly dependent on glucose availability and reducing power generated by pentose phosphate pathway, whereas DCA cotreatment enhanced metformin-cytotoxicity via reprogramming glucose metabolism by inhibiting PDK and increasing mitochondrial respiration. DCA cotreatment elicited cell death rather than cell survival despite high glucose and high GSH condition. In conclusion, DCA sensitized metformin-cytotoxicity by reprogramming glucose metabolism in part from aerobic glycolysis to mitochondrial oxidation, evidenced by measurements of glucose consumption, lactate release, and the ratio of oxygen consumption rate/extracellular acidification rate. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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