原肌球蛋白抑制肿瘤转化和调控细胞骨架。

V Shah, R Braverman, G L Prasad
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引用次数: 30

摘要

原肌球蛋白(TMs)的下调是在许多转化细胞中观察到的一致的生化变化。我们之前的工作已经证明原肌球蛋白-1是一个反基因,它是一个II类肿瘤抑制因子。利用ras转化的小鼠成纤维细胞(DT细胞),我们研究了两种TM亚型的共表达对细胞形态、细胞骨架和致瘤性的影响。TM1(一种转化抑制因子)和TM2(一种非肿瘤抑制因子)的表达增强,可形成组织良好的微丝,其形态类似于正常成纤维细胞,并抑制致瘤性。体内肿瘤的形成与持续高水平的TM2一致,但与高水平的TM1不一致。在这些细胞中观察到TM1和TM2的同型二聚体。因此,在ras转化的细胞中,恢复TM1和TM2蛋白的表达可以抑制转化的表型,并显著地重组微丝。这些数据表明,TM2与TM1共同参与了微丝的重组,而TM1是转化表型的抑制因子。
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Suppression of neoplastic transformation and regulation of cytoskeleton by tropomyosins.

Down regulation of Tropomyosins (TMs) is a consistent biochemical change observed in many transformed cells. Our previous work has demonstrated that Tropomyosin-1 is an antioncogene and it is a class II tumor suppressor. Using ras-transformed murine fibroblasts (DT cells), we have examined the effects of co-expression of two isoforms of TM on cell morphology, cytoskeleton and tumorigenecity. Enhanced expression of TM1, a suppressor of transformation, along with TM2 which is not a tumor suppressor results in the formation of well-organized microfilaments, a morphology that resembles normal fibroblasts, and suppression of tumorigenecity. Tumor formation in vivo was compatible with the persistence of high-level of TM2, but not TM1. Homodimers of TM1 and TM2 were observed in these cells. Thus, restoration of expression of TM1 and TM2 protein in ras-transformed cells suppresses the transformed phenotype with dramatic re-organization of microfilaments. These data show that TM2 cooperates with TM1 in the reorganization of microfilaments, while TM1 is a suppressor of the transformed phenotype.

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