Inhibition of monocarboxylate transporter 1 suppresses the proliferation of glioblastoma stem cells

被引:38
作者
Takada, Tetsuya [1 ]
Takata, Kazuyuki [1 ]
Ashihara, Eishi [1 ]
机构
[1] Kyoto Pharmaceut Univ, Dept Clin & Translat Physiol, Yamashina Ku, 5 Nakauchi, Kyoto 6078414, Japan
关键词
Glioblastoma; Cancer stem cell; Hypoxia; Monocarboxylate transporter; Lactic acid; Carbonic anhydrase; CARBONIC-ANHYDRASE IX; BREAST-CANCER; CD147; PH; IDENTIFICATION; CHEMOTHERAPY; TARGET; GROWTH; MCT2;
D O I
10.1007/s12576-016-0435-6
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Recent evidence suggests that a minor subset of cancer cells, termed cancer stem cells (CSCs), have self-renewal and tumorigenic potential. Therefore, the characterization of CSCs is important for developing therapeutic strategies against cancer. Cancer cells rely on anaerobic glycolysis to produce ATP even under normoxic conditions, resulting in the generation of excess acidic substances. Cancer cells maintain a weakly alkaline intracellular pH to support functions. Glioblastoma is an aggressive malignancy with a poor 5-year survival rate. Based on the hypothesis that ion transport-related molecules regulate the viability and function of CSCs, we investigated the expression of ion transport-related molecules in glioblastoma CSCs (GSCs). Quantitative RT-PCR analysis showed that monocarboxylate transporter1 (MCT1) were upregulated in GSCs, and inhibition of MCT1 decreased the viability of GSCs compared with that of non-GSCs. Our findings indicate that MCT1 is involved in the maintenance of GSCs and is a promising therapeutic target for glioblastoma.
引用
收藏
页码:387 / 396
页数:10
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