miRNA-331-3p directly targets E2F1 and induces growth arrest in human gastric cancer
miRNA-331-3p directly targets E2F1 and induces growth arrest in human gastric cancer
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miRNA-331-3p 直接靶向 E2F1 并诱导人胃癌生长停滞。
DOI：
10.1016/j.bbrc.2010.05.082
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发表时间：
2010-07-16
影响因子：
3.1
通讯作者：
Yu, Yingyan
中科院分区：
文献类型：
--
作者：
Guo, Xiaobo;Guo, Lei;Yu, Yingyan
E2 F1活性失调是胃肿瘤发生的特征，涉及复杂的分子机制。microRNA是基因表达的转录后调节因子之一。在这里，我们报告了miR-331家族的一个成员，miR-331- 3 p，它在某些类型的恶性肿瘤中减少。然而，miR-331- 3 p在胃癌中的生物学功能在很大程度上是未知的。本研究筛选miR-331- 3 p和E2 F1在胃癌细胞系中的表达水平。我们将miR-331- 3 p的前体或抑制剂转染到胃癌细胞中。结果，通过实时PCR，miR-331- 3 p在所有胃癌细胞系中下调。过表达miR-331- 3 p可阻断SGC-7901和AGS细胞的G1/S转换。miR-331- 3 p的引入通过干扰E2 F1活性显著抑制了体外集落形成和细胞生长的能力。我们的数据强调了miR-331- 3 p通过靶向细胞周期相关分子E2 F1的3 '-UTR在细胞周期控制中的重要作用。我们的结论是，miR-331- 3 p是一个潜在的胃癌肿瘤抑制因子。在胃癌细胞中恢复miR-331- 3 p显示了在胃癌治疗中的潜在应用。(C)2010年由Elsevier Inc.出版
Deregulation of E2F1 activity is characteristic of gastric tumorigenesis, which involves in complex molecular mechanisms. microRNA is one of the post-transcriptional regulators for gene expression. Here, we report a member of miR-331 family, miR-331-3p, which was decreased in some kinds of malignancies. However, the biological function of miR-331-3p on gastric cancer is largely unknown. In this study, we screened the expressing levels of miR-331-3p and E2F1 in gastric cancer cell lines. We transfected precursor or inhibitor of miR-331-3p into gastric cancer cells. As results, miR-331-3p is down-regulated in all gastric cancer cell lines by real-time PCR. Over-expression of miR-331-3p blocked G1/S transition on SGC-7901 and AGS cell lines. Introduction of miR-331-3p dramatically suppressed the ability of colony formation and cell growth in vitro by interfering E2F1 activity. Our data highlight an important role of miR-331-3p in cell cycle control by targeting 3'-UTR of cell cycle-related molecule E2F1. We concluded that miR-331-3p is a potential tumor suppressor in gastric cancer. Restoring miR-331-3p in gastric cancer cells revealed potential application in gastric cancer therapy. (C) 2010 Published by Elsevier Inc.