CYTOSKELETAL PROTEINS IN ONCOGENIC TRANSFORMATION AND HUMAN NEOPLASIA

关于原肌球蛋白中错配的作用的研究仍在继续。 (TM)在肿瘤转化中的表达和应用。 逆转录病毒表达后继发的肿瘤转化 癌基因与TM缺乏症的产生相关， 结构上有缺陷的，成纤维细胞和 上皮细胞。这可能是一个基本的结构和功能 有利于细胞内各成分表达的损伤 转化的表型。精神错乱的原因要么是 抑制成纤维细胞的合成和利用，或 由于肌动蛋白(上皮细胞)的相对过度表达。TM 逆转录病毒癌基因转化成纤维细胞的抑制作用可能 是由于α-转化生长因子的作用产生的 作为癌基因表达的结果。TM的表达也是如此 在一组已建立的人类乳腺癌株系中进行了研究。 观察到原肌球蛋白表达的持续异常。 在肿瘤细胞系中，提示TM的排列紊乱 抑制可能是人类乳腺肿瘤的常见事件。

Studies have continued on the role of derangements in tropomyosin (TM) expression and utilization in neoplastic transformation. Neoplastic transformation secondary to expression of retroviral oncogenes is correlated with the production of TM-deficient, structurally defective, microfilaments in both fibroblasts and epithelial cells. This may be a basic structural and functional lesion which is conducive to expression of components of the transformed phenotype. The derangement results either from suppression of synthesis and utilization of TM (fibroblasts), or from relative over-expression of actin (epithelial cells). TM suppression in fibroblasts transformed by retroviral oncogenes may be due to the action of alpha-transforming growth factor produced as a consequence of oncogene expression. TM expression was also studied in a panel of established human breast cancer lines. Consistent abnormalities in tropomyosin expression were observed in the tumor cell lines, suggesting that derangement of TM supression may be a frequent event in human mammary neoplasia.