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有利于表型逆转的基因表达谱:NF-IL6 3'UTR抑制肿瘤机制的线索

Gene expression profile favoring phenotypic reversion: a clue for mechanism of tumor suppression by NF-IL6 3'UTR.

作者信息

Liu Ding Gan, Jiang Qiu Hong, Wei Yun Yi, Sun Li, Fu Bei Bei, Zhao Fu Kun, Zhou Qiong

机构信息

State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

出版信息

Cell Res. 2003 Dec;13(6):509-14. doi: 10.1038/sj.cr.7290195.

DOI:10.1038/sj.cr.7290195
PMID:14728809
Abstract

Transfection of cDNA in 3'untranslated region of human nuclear factor for interleukin-6 (NF-IL6 3'UTR) induced tumor suppression in a human hepatoma cell line. cDNA array analysis was used to reveal changes in gene expression profile leading to tumor suppression The results indicate that this suppression was not due to activation of dsRNA-dependent protein kinase, nor to inactivation of oncogenes; rather, all the changes in expression of known genes, induced by NF-IL6 3'UTR cDNA may be ascribed to the suppression of cellular malignancy. Therefore, our results imply that this 3'untranslated region may have played role of a regulator of gene expression profile.

摘要

在人白细胞介素-6核因子的3'非翻译区(NF-IL6 3'UTR)转染互补DNA(cDNA)可在人肝癌细胞系中诱导肿瘤抑制作用。利用cDNA阵列分析来揭示导致肿瘤抑制的基因表达谱变化。结果表明,这种抑制并非由于双链RNA依赖性蛋白激酶的激活,也不是由于癌基因的失活;相反,由NF-IL6 3'UTR cDNA诱导的已知基因表达的所有变化可能归因于细胞恶性程度的抑制。因此,我们的结果表明,这个3'非翻译区可能起到了基因表达谱调节因子的作用。

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