Effects of Mitochondrial Gene Deletion on Tumorigenicity of Metastatic Melanoma: Reassessing the Warburg Effect
Effects of Mitochondrial Gene Deletion on Tumorigenicity of Metastatic Melanoma: Reassessing the Warburg Effect
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DOI：
10.1089/rej.2009.0948
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发表时间：
2010-04-01
影响因子：
2.6
通讯作者：
Tan, An S.
中科院分区：
文献类型：
--
作者：
Berridge, Michael V.;Tan, An S.
代谢的灵活性是癌症的标志。虽然许多肿瘤优先使用糖酵解在氧气存在下的生物能量的目的（瓦尔堡效应），糖酵解代谢的肿瘤转移的影响还没有被调查。我们采用了一个极端的糖酵解代谢模型来研究转移性B16小鼠黑色素瘤细胞作为原发性皮下肿瘤生长的能力，并在静脉注射到同基因和免疫功能低下的小鼠时形成肺肿瘤。线粒体基因敲除的B16 rho degrees细胞显示出延迟的皮下肿瘤生长，并且令人惊讶的是，未能形成肺肿瘤。结果表明，线粒体活性氧（ROS）可能是肿瘤转移所必需的。
Metabolic flexibility is a hallmark of cancer. Although many tumors preferentially use glycolysis in the presence of oxygen for bioenergetic purposes (Warburg effect), the effects of glycolytic metabolism on tumor metastasis have not been investigated. We have employed an extreme model of glycolytic metabolism to investigate the ability of metastatic B16 mouse melanoma cells to grow as primary subcutaneous tumors and to form lung tumors when injected intravenously into syngeneic and immunocompromised mice. Mitochondrial gene-knockout B16 rho degrees cells showed delayed subcutaneous tumor growth and, surprisingly, failed to form lung tumors. The results suggest that mitochondrial reactive oxygen species (ROS) may be required for tumor metastasis.