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首页> 外文期刊>Cancer Cell >PGC1α Expression Defines a Subset of Human Melanoma Tumors with Increased Mitochondrial Capacity and Resistance to Oxidative Stress.
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PGC1α Expression Defines a Subset of Human Melanoma Tumors with Increased Mitochondrial Capacity and Resistance to Oxidative Stress.

机译：PGC1α表达定义了具有增加的线粒体能力和抗氧化应激能力的人类黑色素瘤肿瘤的子集。

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Cancer cells reprogram their metabolism using different strategies to meet energy and anabolic demands to maintain growth and survival. Understanding the molecular and genetic determinants of these metabolic programs is critical to successfully exploit them for therapy. Here, we report that the oncogenic melanocyte lineage-specification transcription factor MITF drives PGC1α (PPARGC1A) overexpression in a subset of human melanomas and derived cell lines. Functionally, PGC1α positive melanoma cells exhibit increased mitochondrial energy metabolism and reactive oxygen species (ROS) detoxification capacities that enable survival under oxidative stress conditions. Conversely, PGC1α negative melanoma cells are more glycolytic and sensitive to ROS-inducing drugs. These results demonstrate that differences in PGC1α levels in melanoma tumors have a profound impact in their metabolism, biology, and drug sensitivity.
机译：癌细胞使用不同的策略来重新编程其新陈代谢，以满足维持生长和存活所需的能量和合成代谢需求。了解这些代谢程序的分子和遗传决定因素对于成功利用它们进行治疗至关重要。在这里，我们报告致癌的黑素细胞谱系规范转录因子MITF驱动PGC1α（PPARGC1A）在人类黑素瘤和衍生细胞系的子集中过表达。从功能上讲，PGC1α阳性黑色素瘤细胞显示出增加的线粒体能量代谢和活性氧（ROS）解毒能力，从而能够在氧化应激条件下存活。相反，PGC1α阴性的黑色素瘤细胞更具有糖酵解作用，并且对ROS诱导药物敏感。这些结果表明，黑色素瘤肿瘤中PGC1α水平的差异对其代谢，生物学和药物敏感性具有深远影响。

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