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: 3939341
• 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/3939341
• 关键词: carcinogenesis inhibitor; cellular oncology; epithelium; fibroblasts; gene expression; gene redundancy; human tissue; immunosuppression; mouse mammary tumor virus; neoplasm /cancer genetics; neoplastic transformation; transforming growth factors; viral carcinogenesis

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.

有关原肌球蛋白(TM)作用的研究仍在继续 肿瘤转化中的抑制作用。它的作用机制 逆转录病毒癌基因表达抑制TM合成 被探索。我们已经获得了TM抑制的证据 由逆转录病毒癌基因转化的成纤维细胞中的 α-转化生长因子在肿瘤细胞中的作用 癌基因表达的后果。在小鼠的乳房 组成性表达活化c-Ha-ras、TM的上皮细胞 合成没有受到抑制，而是新的积累 合成TM被抑制，显然是由于堆积 肌动蛋白和TM在细胞骨架中的比例异常。TM 研究人员还对一组已建立的人类乳房进行了研究。 癌症线。除1例外，其余均为原肌球蛋白异常 在肿瘤细胞系中观察到表达，表明 TM基因表达紊乱可能是人类的常见事件 肿瘤。