MicroRNA-24 increases hepatocellular carcinoma cell metastasis and invasion by targeting p53: miR-24 targeted p53
MicroRNA-24 increases hepatocellular carcinoma cell metastasis and invasion by targeting p53: miR-24 targeted p53
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MicroRNA-24通过靶向p53增加肝细胞癌细胞转移和侵袭：miR-24靶向p53
DOI：
10.1016/j.biopha.2016.10.051
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发表时间：
2016-12-01
影响因子：
7.5
通讯作者：
Huang, Xiao-Hui
中科院分区：
文献类型：
--
作者：
Chen, Li;Luo, Liang;Huang, Xiao-Hui
microRNA-24（miR-24）是miRNA家族的成员，在各种类型的人类癌症中作为癌基因发挥作用。然而，miR-24参与肝细胞癌（HCC）发生和进展的潜在机制仍知之甚少。本研究基于荧光素酶报告基因分析揭示了miRNA-24通过与p53 mRNA的3 '-UTR结合下调p53，并且miR-24的表达水平可以通过p53影响HCC细胞系的侵袭。p53的下调显著减弱了miR-24敲低对HCC细胞侵袭的抑制作用，提示miR-24可能是HCC治疗的潜在靶点。此外，我们的研究结果显示，与匹配的非转移性肿瘤组织相比，miR-24在HCC转移性肿瘤组织中的表达显著增加，并且miR-24的上调与HCC组织中p53的下调显著相关。总之，这项研究表明，miR-24作为癌基因在HCC中发挥作用，至少部分通过下调p53促进细胞侵袭。因此，miR-24可能成为肝癌治疗的潜在靶点。(C)2016 Elsevier Masson SAS。All rights reserved.
MicroRNA-24 (miR-24), a member of the miRNA family, functions as an oncogene in various types of human cancer. However, the underlying mechanisms of miR-24 involvement in the development and progression of hepatocellular carcinoma (HCC) remain poorly understood. The present study revealed that miRNA-24 down-regulates p53 through binding to the 3 '-UTR of p53 mRNA based on a luciferase reporter assay, and that the expression level of miR-24 could affect the invasion of HCC lines via p53. Down-regulation of p53 significantly attenuated the inhibitory effects of miR-24 knockdown on the invasion of HCC cells, suggesting that miR-24 could be a potential target for HCC treatment. Moreover, our results revealed that miR-24 expression was significantly increased in HCC metastatic tumor tissues compared with matched non-metastatic tumor tissues, and that the up-regulation of miR-24 was significantly associated with down-regulation of p53 in the HCC tissues. In conclusion, this study demonstrates that miR-24 functions as an oncogene in HCC, at least partly by promoting cell invasion through down-regulation of p53. Therefore, miR-24 may be a potential therapeutic target for treatment of HCC. (C) 2016 Elsevier Masson SAS. All rights reserved.