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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Adenovirus-mediated suppression of HMGl(Y) protein synthesis as potential therapy of human malignant neoplasias
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Adenovirus-mediated suppression of HMGl(Y) protein synthesis as potential therapy of human malignant neoplasias

机译：腺病毒介导的HMG1（Y）蛋白质合成抑制作为人类恶性肿瘤的潜在治疗方法

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摘要

High mobility group l (HMGl) proteins are overexpressed in several human malignant tumors. We previously demonstrated that inhibi- tion of HMGl synthesis prevents thyroid cell transformation. Here, we report that an adenovirus carrying the HMGI(Y) gene in an antisense orientation (Ad-Yas) induced programmed cell death of two human thyroid anaplastic carcinoma cell lines (ARO and FB-1), but not normal thyroid cells. The Ad-Yas virus led to death of lung, colon. and breast carcinoma cells. A control adenovirus carrying the laCZ gene did not inhibit the growth of either normal or neoplastic cells. Ad-Yas treat- ment of tumors induced in athymic mice by ARO cells caused a drastic reduction in tumor size. Therefore, suppression of HMGl(Y) protein synthesis by an HMGl(Y) antisense adenoviral vector may be a useful treatment strategy in a variety of human malignant neoplasias, in which HMGl(Y) gene overexpression is a general event.
机译：高迁移性I族（HMG1）蛋白在几种人类恶性肿瘤中过表达。我们先前证明抑制HMG1合成可以阻止甲状腺细胞转化。在这里，我们报告腺病毒以反义方向（Ad-Yas）携带HMGI（Y）基因诱导了两种人类甲状腺间变性癌细胞系（ARO和FB-1）的程序性细胞死亡，但没有正常的甲状腺细胞。 Ad-Yas病毒导致肺，结肠死亡。和乳腺癌细胞。带有laCZ基因的对照腺病毒不抑制正常或肿瘤细胞的生长。 Ad-Yas治疗ARO细胞在无胸腺小鼠中引起的肿瘤，导致肿瘤大小急剧减少。因此，通过HMG1（Y）反义腺病毒载体抑制HMG1（Y）蛋白合成可能是多种人类恶性肿瘤中有用的治疗策略，其中HMG1（Y）基因过表达是普遍事件。

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