Bryant Kirsten L, Der Channing J
Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7295, USA.
Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7295, USA.
Dev Cell. 2017 Jan 23;40(2):120-122. doi: 10.1016/j.devcel.2017.01.005.
Mutant RAS-driven cancers are infamously resistant to chemotherapeutics. Reporting in Cell, Grabocka and Bar-Sagi (2016) demonstrate that when subjected to stress, mutant KRAS-dependent lipid production leads to upregulated stress granule formation. This confers not only cell-autonomous cytoprotection but also paracrine establishment of a stress-resistant tumor niche.
突变型RAS驱动的癌症对化疗具有众所周知的抗性。Grabocka和Bar-Sagi(2016年)在《细胞》杂志上发表的报告表明,在受到应激时,依赖突变型KRAS的脂质生成会导致应激颗粒形成上调。这不仅赋予细胞自主性细胞保护作用,还能通过旁分泌建立抗应激肿瘤微环境。