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Cancer cells gain a growth advantage through the so-called Warburg effect by shifting glucose metabolism from oxidative phosphorylation to aerobic glycolysis. Hypoxia-inducible factor 1 (HIF-1) has been suggested to function in metabolic reprogramming; however, the underlying mechanism has not been fully elucidated. We found that the aberrant expression of wild-type isocitrate dehydrogenase 3α (IDH3α), a subunit of the IDH3 heterotetramer, decreased α-ketoglutarate levels and increased the stability and transactivation activity of HIF-1α in cancer cells. The silencing of IDH3α significantly delayed tumor growth by suppressing the HIF-1-mediated Warburg effect and angiogenesis. IDH3α expression was associated with the poor postoperative overall survival of lung and breast cancer patients. These results justify the exploitation of IDH3 as a novel target for the diagnosis and treatment of cancers.

Original publication




Journal article



Publication Date





4758 - 4766


Animals, Breast Neoplasms, Cell Line, Tumor, Cell Proliferation, Female, Gene Expression Regulation, Neoplastic, Glucose, Glycolysis, Humans, Hypoxia-Inducible Factor 1, alpha Subunit, Isocitrate Dehydrogenase, Lung Neoplasms, Mice, Neovascularization, Pathologic, Oxidative Phosphorylation