CYTOSKELETAL PROTEINS IN ONCOGENIC TRANSFORMATION AND HUMAN NEOPLASIA

关于原肌球蛋白（TM）的作用的研究仍在继续。 抑制肿瘤转化。 的机理 通过逆转录病毒癌基因表达抑制TM合成， 正在探索中。 我们有证据表明TM抑制 逆转录病毒癌基因转化的成纤维细胞中的细胞凋亡是由于 α-转化生长因子作为一种 癌基因表达的结果。 小鼠乳腺 组成型表达激活的c-Ha-ras，Tm的上皮细胞 合成没有受到抑制，但新的 合成TM被抑制，显然是由于积累 肌动蛋白和TM在细胞骨架中的比例异常。 TM 还在一组已建立的人乳腺癌组织中研究了表达。 癌细胞系 除1例外，所有病例原肌球蛋白异常 在肿瘤细胞系中观察到表达，表明 TM表达紊乱可能是人类中常见事件 肿瘤形成

Studies have continued on the role of tropomyosin (TM) suppression in neoplastic transformation. The mechanism of suppression of TM synthesis by retroviral oncogene expression is being explored. We have obtained evidence that TM suppression in fibroblasts transformed by retroviral oncogenes is due to the action of alpha-transforming growth factor produced as a consequence of oncogene expression. In mouse mammary epithelial cells constitutively expressing activated c-Ha-ras, Tm synthesis was not suppressed, but accumulation of newly synthesized TM was suppressed, apparently due to accumulation of actin and TM in abnormal ratios in the cytoskeleton. TM expression was also studied in a panel of established human breast cancer lines. In all but one case abnormalities in tropomyosin expression were observed in the tumor cell lines, suggesting that derangement of TM expression may be a frequent event in human neoplasia.