突变KRAS驱动肿瘤中的代谢网络:组织特异性和微环境
Metabolic networks in mutant KRAS-driven tumours: tissue specificities and the microenvironment
原文发布日期:2021-07-09
DOI: 10.1038/s41568-021-00375-9
类型: Review Article
开放获取: 否
英文摘要:
摘要翻译:
原文链接:
Oncogenic mutations in KRAS drive common metabolic programmes that facilitate tumour survival, growth and immune evasion in colorectal carcinoma, non-small-cell lung cancer and pancreatic ductal adenocarcinoma. However, the impacts of mutant KRAS signalling on malignant cell programmes and tumour properties are also dictated by tumour suppressor losses and physiological features specific to the cell and tissue of origin. Here we review convergent and disparate metabolic networks regulated by oncogenic mutant KRAS in colon, lung and pancreas tumours, with an emphasis on co-occurring mutations and the role of the tumour microenvironment. Furthermore, we explore how these networks can be exploited for therapeutic gain.
KRAS致癌突变驱动共同的代谢程序,促进结直肠癌、非小细胞肺癌和胰腺导管腺癌中肿瘤的存活、生长及免疫逃逸。然而,突变KRAS信号对恶性细胞程序及肿瘤特性的影响还取决于抑癌基因的缺失以及细胞和组织来源特有的生理特征。本文综述了结肠、肺和胰腺肿瘤中由致癌突变KRAS调控的趋同及差异性代谢网络,重点探讨共存突变的作用及肿瘤微环境的影响。此外,我们还探索了如何利用这些网络实现治疗获益。
Metabolic networks in mutant KRAS-driven tumours: tissue specificities and the microenvironment
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