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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >ETS1 suppresses tumorigenicity of human colon cancer cells.
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ETS1 suppresses tumorigenicity of human colon cancer cells.

机译：ETS1抑制人类结肠癌细胞的致瘤性。

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摘要

We have ectopically expressed transcription factor ETS1 in two different highly tumorigenic human colon cancer cell lines, DLD-1 and HCT116, that do not express endogenous ETS1 protein and have obtained several independent clones. The expression of wild-type ETS1 protein in these colon cancer cells reverses the transformed phenotype and tumorigenicity in a dose-dependent manner. By contrast, expression in DLD-1 cells of a variant form of ETS1, lacking transcriptional activity, did not alter the tumorigenic properties of the cells, suggesting that the reduction in tumorigenicity in these clones was specific for the wild-type ETS1 gene products. Since these colon cancer cells have multiple genetic alterations, the system described in this paper could be a good model to study the suppression of tumorigenicity at a transcriptional level, which could lead to the design and development of novel drugs for cancer treatment.
机译：我们已经异位表达转录因子ETS1在两种不同的高度致瘤性人类结肠癌细胞系DLD-1和HCT116中，它们不表达内源性ETS1蛋白，并获得了几个独立的克隆。这些结肠癌细胞中野生型ETS1蛋白的表达以剂量依赖性方式逆转了转化的表型和致瘤性。相比之下，缺乏转录活性的ETS1变体形式在DLD-1细胞中的表达不会改变细胞的致瘤特性，这表明这些克隆的致瘤性降低对野生型ETS1基因产物具有特异性。由于这些结肠癌细胞具有多种遗传改变，因此本文描述的系统可能是研究在转录水平抑制致癌性的良好模型，这可能导致设计和开发用于癌症治疗的新药。

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