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首页> 外文期刊>Molecular and Cellular Biology >The oncogenic forms of N-ras or H-ras prevent skeletal myoblast differentiation.
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The oncogenic forms of N-ras or H-ras prevent skeletal myoblast differentiation.

机译：N-ras或H-ras的致癌形式可阻止骨骼肌成肌细胞分化。

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Differentiation of skeletal muscle involves withdrawal of myoblasts from the cell cycle, fusion to form myotubes, and the coordinate expression of a variety of muscle-specific gene products. Fibroblast growth factor and type beta transforming growth factor specifically inhibit myogenesis; however, the transmembrane signaling pathways responsible for suppression of differentiation by these growth factors remain elusive. Because ras proteins have been implicated in the transduction of growth factor signals across the plasma membrane, we used DNA-mediated gene transfer to investigate the potential involvement of this family of regulatory proteins in the control of myogenesis. Transfection of the mouse skeletal muscle cell line C2 with the oncogenic forms of H-ras or N-ras completely suppressed both myoblast fusion and induction of the muscle-specific gene products nicotinic acetylcholine receptor and creatine kinase. Inhibition of differentiation by activated ras genes occurred at the level of muscle-specific mRNA accumulation. In contrast, proto-oncogenic forms of N-ras or H-ras had no apparent effects on the ability of C2 cells to differentiate. Myoblasts transfected with activated ras genes exhibited normal growth properties and ceased proliferating in the absence of mitogens, indicating that ras inhibited differentiation through a mechanism independent of cell proliferation. These results demonstrate that activated ras gene products mimic the inhibitory effects of fibroblast growth factor and type beta transforming growth factor on myogenic differentiation and suggest that each of these regulators of myogenesis may operate through a common intracellular pathway.
机译：骨骼肌的分化涉及成肌细胞从细胞周期中退出，融合形成肌管以及各种肌肉特异性基因产物的协调表达。成纤维细胞生长因子和β型转化生长因子特异性抑制肌发生。但是，负责抑制这些生长因子分化的跨膜信号通路仍然难以捉摸。因为ras蛋白已经牵涉到跨质膜的生长因子信号的转导中，所以我们使用DNA介导的基因转移来研究这一调节蛋白家族在肌发生控制中的潜在参与。用致癌形式的H-ras或N-ras转染小鼠骨骼肌细胞系C2完全抑制了成肌细胞融合以及肌肉特异性基因产物烟碱型乙酰胆碱受体和肌酸激酶的诱导。活化的ras基因抑制分化发生在肌肉特异性mRNA积累水平。相反，原癌形式的N-ras或H-ras对C2细胞的分化能力没有明显影响。转染了活化的ras基因的成肌细胞表现出正常的生长特性，并且在不存在有丝分裂原的情况下停止增殖，这表明ras通过独立于细胞增殖的机制抑制了分化。这些结果表明，活化的ras基因产物模拟了成纤维细胞生长因子和β型转化生长因子对肌原性分化的抑制作用，并暗示了每个这些肌原性调节因子都可以通过共同的细胞内途径起作用。

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