Prasad G L
Department of General Surgery, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.
Methods Enzymol. 2006;407:410-22. doi: 10.1016/S0076-6879(05)07034-5.
Neoplastic transformation by Ras proteins markedly suppresses the expression of certain isoforms of tropomyosins (TMs), which are important regulators of actin cytoskeleton. Downregulation of TMs and other actin-associated proteins is believed to result in the assembly of aberrant cytoskeleton, which in turn contributes to the malignant transformation by Ras. Oncogenic activation of ras, in addition to suppressing TMs by means of epigenetic mechanisms, also rapidly inhibits their cytoskeletal fractionation, leading to the disruption of cytoskeleton. Restoration of expression of certain isoforms of TMs reorganizes microfilaments and suppresses the malignant growth of ras-transformed cells. This chapter discusses some of the approaches to the analysis of TM isoform expression in normal and ras-transformed cells.
Ras蛋白介导的肿瘤转化显著抑制了某些原肌球蛋白(TMs)亚型的表达,而TMs是肌动蛋白细胞骨架的重要调节因子。TMs及其他肌动蛋白相关蛋白的下调被认为会导致异常细胞骨架的组装,进而促进Ras介导的恶性转化。Ras的致癌激活除了通过表观遗传机制抑制TMs外,还会迅速抑制其细胞骨架的分离,导致细胞骨架的破坏。某些TMs亚型表达的恢复可重组微丝并抑制Ras转化细胞的恶性生长。本章讨论了一些分析正常细胞和Ras转化细胞中TM亚型表达的方法。