FAK 来救援：激活的基质通过诱导 FAK 信号促进 BRAF 突变型黑素瘤细胞的“避难所”形成。
FAK to the rescue: activated stroma promotes a "safe haven" for BRAF-mutant melanoma cells by inducing FAK signaling.
机构信息
Cancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK.
Cancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK.
出版信息
Cancer Cell. 2015 Apr 13;27(4):429-31. doi: 10.1016/j.ccell.2015.03.013.
Perhaps the most pressing need in cancer therapeutics is to understand drug resistance. In this issue of Cancer Cell, Hirata and colleagues show that melanoma-associated fibroblasts can drive resistance to the BRAF inhibitor PLX4720 by stimulating matrix production/remodeling, and, consequently, survival signaling in melanoma cells via β1-integrin, Src, and FAK.
或许癌症治疗中最紧迫的需求是理解药物耐药性。在本期《癌细胞》中，平田等人表明，黑色素瘤相关成纤维细胞可以通过刺激基质产生/重塑，以及随后通过β1 整合素、Src 和 FAK 刺激黑色素瘤细胞的存活信号，来驱动 BRAF 抑制剂 PLX4720 的耐药性。
Zotero 插件