Growth inhibition of human hepatocellular carcinoma cells by blocking STAT3 activation with decoy-ODN
Growth inhibition of human hepatocellular carcinoma cells by blocking STAT3 activation with decoy-ODN
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用诱饵-ODN 阻断 STAT3 激活抑制人肝癌细胞的生长
DOI：
10.1016/j.canlet.2007.12.009
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发表时间：
2008-04-18
期刊：
影响因子：
9.7
通讯作者：
Tian, Zhigang
中科院分区：
文献类型：
--
作者：
Sun, Xiaoxia;Zhang, Jian;Tian, Zhigang
越来越多的研究表明，信号转导子和转录激活子3（STAT 3）在多种恶性肿瘤中被组成性激活，成为肿瘤治疗的重要分子靶点。本研究采用特异性阻断过活化的STAT 3的STAT 3-decoy ODN处理人肝癌细胞，观察其体外增殖能力并探讨其分子机制。结果表明，STAT 3-decoy ODN能显著抑制肝癌细胞的增殖，并使肝癌细胞凋亡增加，细胞阻滞于G 0/G1期向S期转变。进一步的研究发现，STAT 3调控的细胞凋亡和细胞周期进程相关基因bcl-x1、cyclin D1和c-myc在转录和翻译水平上表达均显著下调。这些数据表明，STAT 3可能被用作HCC治疗的分子靶点。(C)2007爱思唯尔爱尔兰有限公司保留所有权利。
More and more studies show that signal transducer and activator of transcription 3 (STAT3) is frequently constitutively activated in a wide number of malignancies and named as an attractive molecular target for tumor treatment. Here, we employed STAT3-decoy ODN, which specifically block over-activated STAT3, to treat human hepatocellular carcinoma (HCC) cells, and evaluated the cellular proliferation ability and investigated the molecular mechanisms in vitro. The results demonstrated that the proliferation of HCC cells was suppressed significantly by STAT3-decoy ODN, being associated with the increased apoptosis and cell arrest at G0/G1 to S phase transition. Further investigates showed the expression of STAT3-regulated genes including bcl-x1, cyclin D1 and c-myc, which involved in cell apoptosis and cell cycle progression, were down-regulated significantly both at transcription and translation levels. These data suggested that STAT3 may be potentially used as a molecular target in HCC therapy. (C) 2007 Elsevier Ireland Ltd. All rights reserved.