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mTORC2 dictates Warburg effect and drug resistance

机译：mTORC2决定了Warburg的作用和耐药性

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Metabolic reprogramming, a prominent phenotype in cancer cells, is the adaptation to shifts in the usage of metabolites, including glucose, fatty acids, amino acids, and glutamine. The central feature of this adaptation lies in the fact that cancer cells undergo glycolysis even in the presence of ample oxygen, contrary to normal cells.1 This aerobic glycolysis, termed "the Warburg effect," has been considered to give tumor cells selective advantages through enhanced catabolism of glucose and glutamine, providing the raw materials for the synthesis of nucleotides, amino acids, and lipids to satiate rapidly dividing cancer cells. On the other side of the coin, however, unravelling the molecular network that dictates the Warburg effect may be potentially exploited for identifying new drug targets and drug resistance mechanisms in cancer.
机译：代谢重编程是癌细胞中一个显着的表型，是对代谢物（包括葡萄糖，脂肪酸，氨基酸和谷氨酰胺）使用量变化的适应。这种适应的主要特征在于，即使在充足的氧气存在下，癌细胞也会发生糖酵解，这与正常细胞相反。1这种有氧糖酵解（称为“ Warburg效应”）被认为可以通过以下方式为肿瘤细胞提供选择优势：增强了葡萄糖和谷氨酰胺的分解代谢，为合成核苷酸，氨基酸和脂质提供了满足快速分裂的癌细胞所需的原料。然而，在硬币的另一面，揭示沃堡效应的分子网络可能被潜在地用于识别癌症中的新药物靶标和耐药机制。

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