MicroRNA 483-3p suppresses the expression of DPC4/Smad4 in pancreatic cancer
MicroRNA 483-3p suppresses the expression of DPC4/Smad4 in pancreatic cancer
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DOI：
10.1016/j.febslet.2010.11.039
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发表时间：
2011-01-03
期刊：
影响因子：
3.5
通讯作者：
Shao, Chenghao
中科院分区：
文献类型：
--
作者：
Hao, Jun;Zhang, Shuyu;Shao, Chenghao
肿瘤抑制基因的失调和microRNAs（miRNAs）的错误表达都与胰腺癌的发生有关，但在此过程中它们之间的关系尚不清楚。在这里，我们报告说，miR-483- 3 p的表达强烈增强胰腺癌组织相比，侧正常组织使用miRNA阵列差异分析。此外，DPC 4/Smad 4被鉴定为miR-483- 3 p的靶标，并且它们的表达水平在人类临床标本中呈负相关。miR-483- 3 p的异位表达显著抑制胰腺癌细胞系中DPC 4/Smad 4蛋白水平，同时促进细胞增殖和体外集落形成。我们的研究结果确定miR-483- 3 p作为DPC 4/Smad 4的有效调节剂，这可能为治疗DPC 4/Smad 4驱动的胰腺癌提供新的治疗策略。(C)2010年欧洲生物化学学会联合会。由Elsevier B出版。V.保留所有权利。
Both deregulation of tumor-suppressor genes and misexpression of microRNAs (miRNAs) have been implicated in the development of pancreatic cancer, but their relationship during this process remains less clear. Here, we report that the expression of miR-483-3p is strongly enhanced in pancreatic cancer tissues compared to side normal tissues using a miRNA-array differential analysis. Furthermore, DPC4/Smad4 is identified as a target of miR-483-3p and their expression levels are inversely correlated in human clinical specimens. Ectopic expression of miR-483-3p significantly represses DPC4/Smad4 protein levels in pancreatic cancer cell lines, and simultaneously promotes cell proliferation and colony formation in vitro. Our findings identify miR-483-3p as a potent regulator of DPC4/Smad4, which may provide a novel therapeutic strategy for the treatment of DPC4/Smad4-driven pancreatic cancer. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.