MicroRNA-184 inhibits cell proliferation and invasion, and specifically targets TNFAIP2 in Glioma.
MicroRNA-184 inhibits cell proliferation and invasion, and specifically targets TNFAIP2 in Glioma.
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MicroRNA-184 抑制细胞增殖和侵袭，并特异性靶向胶质瘤中的 TNFAIP2
DOI：
10.1186/s13046-015-0142-9
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发表时间：
2015-03-26
期刊：
影响因子：
--
通讯作者：
Zhou Y
中科院分区：
文献类型：
--
作者：
Cheng Z;Wang HZ;Li X;Wu Z;Han Y;Li Y;Chen G;Xie X;Huang Y;Du Z;Zhou Y
miRNA-184是人肝细胞癌中的癌基因，但在舌鳞状细胞癌中作为肿瘤抑制基因。研究表明，miR-184在胶质瘤中表达下调，TNFα诱导蛋白2（TNFAIP 2）与胶质瘤的发生密切相关。本研究旨在探讨miR-184在胶质瘤中的作用以及miRNA-184-TNFAIP 2介导胶质瘤进展的机制。实时逆转录PCR检测miR-184和TNFAIP 2的表达。用miR-184模拟物、抑制剂或阴性对照miRNA转染U87和U251细胞，并测定其侵袭能力。通过细胞计数试剂盒-8测定法测量细胞增殖。流式细胞仪检测miR-184对胶质瘤细胞凋亡和细胞周期的影响。生物信息学软件预测miR-184可以靶向TNFα诱导蛋白2（TNFAIP 2），并在胶质瘤细胞中通过Western blot和qRT-PCR进一步验证。在体内，将用慢病毒过表达miR-184或对照慢病毒转导的U87细胞分别皮下和颅内注射到裸鼠中。与正常脑组织相比，miR-184在胶质瘤组织和细胞系中的表达显著降低。胶质瘤中TNFAIP 2的蛋白和mRNA表达与miR-184呈负相关。在体外，用miR-184模拟物转染后，U87和U251细胞的增殖和侵袭能力也降低。在体内，miR-184过表达组中的异种移植肿瘤尺寸小于miR-NC组。一致地，用miR-184模拟物转染的U87和U251细胞具有更高的凋亡率，触发G 0/G1期细胞的积累和S期细胞的减少。miR-184可调节TNFAIP 2在胶质瘤中的表达并影响其翻译。miR-184还可以抑制胶质瘤的进展，可能成为胶质瘤治疗的新靶点。本文的在线版本（doi：10.1186/s13046-015-0142-9）包含补充材料，可供授权用户使用。
miRNA-184 is an oncogene in human hepatocellular carcinoma but acts as a tumor suppressor in tongue squamous cell carcinoma. Studies have shown that miR-184 was down-regulated in glioma and TNFα-induced protein 2 (TNFAIP2) was closely related to tumorigenesis. This study aimed to determine the functions of miR-184 in glioma and the mechanisms of miRNA-184-TNFAIP2 mediated glioma progression. Real-time reverse-transcription PCR detected expression of miR-184 and TNFAIP2. U87 and U251 cells were transfected with miR-184 mimic, inhibitor, or negative control miRNA, and their invasion abilities were assayed. Cellular proliferation was measured by the cell counting kit-8 assay. miR-184 effects on glioma cell apoptosis and cell cycle were assessed by flow cytometer. Biological information software have predicted that miR-184 could target TNFα-induced protein 2 (TNFAIP2), Which was further validated by Western blot and qRT-PCR in glioma cells. In vivo, U87 cells transduced with either lentiviral over-expressed miR-184 or control lentivirus were injected into nude mice subcutaneously and intracranial respectively. Expression of miR-184 was significantly lower in glioma tissues and cell-lines compared to normal brain tissues. Protein and mRNA expression of TNFAIP2 were inversely correlated with miR-184 in glioma. In vitro, proliferation and invasion abilities were also decreased in U87 and U251 cells after transfection with miR-184 mimic. In vivo, the xenografted tumor size in the miR-184 overexpressing group were smaller than the miR-NC group. Concordantly, U87 and U251 cells transfected with miR-184 mimic had a higher apoptosis rate, triggering an accumulation of cells at the G0/G1 phase and decreased cells in S-phase. miR-184 could regulate TNFAIP2 expression and affected its translation in glioma. miR-184 could also inhibit glioma progression and might serve as a novel therapeutic target in glioma. The online version of this article (doi:10.1186/s13046-015-0142-9) contains supplementary material, which is available to authorized users.
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DOI：
10.1186/1756-9966-31-97
发表时间：
2012-11-22
期刊：
Journal of experimental & clinical cancer research : CR
影响因子：
--
作者：
Wang Q;Li P;Li A;Jiang W;Wang H;Wang J;Xie K
通讯作者：
Xie K
影响因子：
7.5
作者：
Chen, Lih-Chyang;Chen, Chia-Chun;Hsueh, Chuen
通讯作者：
Hsueh, Chuen
影响因子：
8
作者：
Lee, K-H;Chen, Y-L;Lu, P-J
通讯作者：
Lu, P-J
肿瘤抑制因子 PDCD4 调节 miR-184 介导的 C-MYC 和 BCL2 直接抑制，从而阻断鼻咽癌细胞的生长和存活。
影响因子：
9
作者：
Zhen, Yan;Liu, Zhen;Yang, Huiling;Yu, Xiaoli;Wu, Qiangyun;Hua, Shengni;Long, Xiaobin;Jiang, Qingping;Song, Ye;Cheng, Chao;Wang, Hao;Zhao, Menyang;Fu, Qiaofen;Lyu, Xiaoming;Chen, Yiyu;Fan, Yue;Liu, Yan;Li, Xin;Fang, Weiyi
通讯作者：
Fang, Weiyi
影响因子：
4.1
作者：
Lacroix, M;Abi-Said, D;Sawaya, R
通讯作者：
Sawaya, R