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线粒体基因缺失对转移性黑色素瘤致瘤性的影响:重新评估沃伯格效应。

Effects of mitochondrial gene deletion on tumorigenicity of metastatic melanoma: reassessing the Warburg effect.

机构信息

Malaghan Institute of Medical Research, Wellington, New Zealand.

出版信息

Rejuvenation Res. 2010 Apr-Jun;13(2-3):139-41. doi: 10.1089/rej.2009.0948.

DOI:10.1089/rej.2009.0948
PMID:20370492
Abstract

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 B16rho 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.

摘要

代谢灵活性是癌症的一个标志。尽管许多肿瘤在有氧条件下优先利用糖酵解来进行生物能量目的(Warburg 效应),但糖酵解代谢对肿瘤转移的影响尚未被研究过。我们采用了一种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的生长能力,以及当它们被静脉注射到同种和免疫缺陷小鼠中时形成肺肿瘤的能力。线粒体基因敲除的 B16rho 度细胞显示出皮下肿瘤生长的延迟,而且令人惊讶的是,它们未能形成肺肿瘤。结果表明,线粒体活性氧(ROS)可能是肿瘤转移所必需的。

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