CYTOSKELETAL PROTEINS IN ONCOGENIC TRANSFORMATION AND HUMAN NEOPLASIA

致癌转化和人类肿瘤中的细胞骨架蛋白

• 批准号: 3916370
• 负责人: H L COOPER
• 金额: --
• 依托单位: DIVISION OF CANCER BIOLOGY AND DIAGNOSIS
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3916370
• 关键词: actins; breast neoplasms; cellular oncology; cytoskeleton; epithelium; fibroblasts; gene expression; human subject; laboratory mouse; microfilaments; mouse mammary tumor virus; neoplasm /cancer genetics; neoplastic cell; neoplastic transformation; oncogenes; transforming growth factors; tropomyosin; viral carcinogenesis

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.

关于原肌球蛋白紊乱的作用的研究仍在继续 (TM)在肿瘤转化中的表达和利用。 继发于逆转录病毒表达的肿瘤性转化 癌基因与TM缺陷的产生相关， 纤维母细胞中存在结构缺陷的微丝， 上皮细胞 这可能是一个基本的结构和功能 病变，这有助于表达的组成部分， 转化表型 这种紊乱要么是由于 抑制TM（成纤维细胞）的合成和利用，或 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的成纤维细胞中的抑制可能 是由于α-转化生长因子的作用而产生的 这是癌基因表达的结果。 TM表达也 在一组已建立的人类乳腺癌细胞系中进行了研究。 观察到原肌球蛋白表达的一致异常， 在肿瘤细胞系中，这表明TM的紊乱 抑制可能是人类乳腺肿瘤中常见事件。