期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 118, 期 12, 页码 3835-3837出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI37373
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资金
- NHLBI NIH HHS [N01-HV28180, P01-HL65608, R01-HL55338, N01HV28180, R01 HL055338, P01 HL065608] Funding Source: Medline
- NIGMS NIH HHS [P20 GM078494, P20-GM78494] Funding Source: Medline
Tumors contain well-oxygenated (aerobic) and poorly oxygenated (hypoxic) regions, which were thought to utilize glucose for oxidative and glycolytic metabolism, respectively. In this issue of the JCI, Sonveaux et al. show that human cancer cells cultured under hypoxic conditions convert glucose to lactate and extrude it, whereas aerobic cancer cells take up lactate via monocarboxylate transporter 1 (MCT1) and utilize it for oxidative phosphorylation (see the related article beginning on page 3930). When MCT1 is inhibited, aerobic cancer cells take up glucose rather than lactate, and hypoxic cancer cells die due to glucose deprivation. Treatment of tumor-bearing mice with an inhibitor of MCT1 retarded tumor growth. MCTI expression was detected exclusively in nonhypoxic regions of human cancer biopsy samples, and in combination, these data suggest that MCT1 inhibition holds potential as a novel cancer therapy.
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