Tumor metabolism of malignant gliomas.
Tumor metabolism of malignant gliomas.
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DOI：
10.3390/cancers5041469
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发表时间：
2013-11-08
期刊：
影响因子：
5.2
通讯作者：
Guo D
中科院分区：
文献类型：
--
作者：
Ru P;Williams TM;Chakravarti A;Guo D
EGFR/PI3K/Akt和Ras/RAF/MEK通路等基因突变构成性激活的致癌信号已被认为是大多数癌症发生的主要驱动因素。最近对肿瘤代谢的研究进一步表明，致癌信号通路直接促进代谢重编程，上调脂质、碳水化合物、蛋白质、DNA和RNA的生物合成，从而促进人类肿瘤的生长。因此，靶向细胞代谢已成为肿瘤药物开发的新方向。在恶性胶质瘤中，葡萄糖、谷氨酰胺和脂质的代谢途径明显重编程。此外，引起这些代谢变化的分子机制才刚刚开始被揭示。在这篇综述中，我们将总结最近的研究揭示了导致恶性胶质瘤代谢变化的关键基因改变，并讨论了通过靶向代谢调节的关键参与者的有希望的治疗策略。
Constitutively activated oncogenic signaling via genetic mutations such as in the EGFR/PI3K/Akt and Ras/RAF/MEK pathways has been recognized as a major driver for tumorigenesis in most cancers. Recent insights into tumor metabolism have further revealed that oncogenic signaling pathways directly promote metabolic reprogramming to upregulate biosynthesis of lipids, carbohydrates, protein, DNA and RNA, leading to enhanced growth of human tumors. Therefore, targeting cell metabolism has become a novel direction for drug development in oncology. In malignant gliomas, metabolism pathways of glucose, glutamine and lipid are significantly reprogrammed. Moreover, molecular mechanisms causing these metabolic changes are just starting to be unraveled. In this review, we will summarize recent studies revealing critical gene alterations that lead to metabolic changes in malignant gliomas, and also discuss promising therapeutic strategies via targeting the key players in metabolic regulation.