Suppr超能文献

miR-219 通过靶向 CD164 抑制髓母细胞瘤细胞的增殖、迁移和侵袭。

miR-219 inhibits the proliferation, migration and invasion of medulloblastoma cells by targeting CD164.

机构信息

Department of Psychiatry, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.

Tianyou Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, Hubei 430081, P.R. China.

出版信息

Int J Mol Med. 2014 Jul;34(1):237-43. doi: 10.3892/ijmm.2014.1749. Epub 2014 Apr 22.

Abstract

It is known that microRNA-219 (miR-219) expression is downregulated in medulloblastoma. In the present study, we investigated the expression, targets and functional effects of miR-219 in D283-MED medulloblastoma cells. We first demonstrated that miR-219 not only inhibits proliferation, but also suppresses the invasion and migration of D283-MED cells. Moreover, the knockdown of miR-219 promoted the proliferation, migration and invasion of the D283-MED cells. Secondly, we predicted that miR-219 targets the 3' untranslated region (3'UTR) of CD164 and orthodenticle homeobox 2 (OTX2) and then confirmed that it significantly downregulated the protein expression of CD164 and OTX2 in D283-MED cells. Finally, we demonstrated that the proliferation, invasion and migration of D283-MED cells were promoted by theectopic expression of CD164. These results indicate that miR-219 suppresses the proliferation, migration and invasion of medulloblastoma cells by targeting CD164. The results also suggest that miR-219 may serve as a potential therapeutic agent for medulloblastoma.

摘要

已知微小 RNA-219(miR-219)在髓母细胞瘤中的表达下调。在本研究中,我们研究了 miR-219 在 D283-MED 髓母细胞瘤细胞中的表达、靶标和功能效应。我们首先证明 miR-219 不仅抑制增殖,还抑制 D283-MED 细胞的侵袭和迁移。此外,miR-219 的敲低促进了 D283-MED 细胞的增殖、迁移和侵袭。其次,我们预测 miR-219 靶向 CD164 和同源盒蛋白 2(OTX2)的 3'非翻译区(3'UTR),然后证实它显著下调了 D283-MED 细胞中 CD164 和 OTX2 的蛋白表达。最后,我们证明 CD164 的异位表达促进了 D283-MED 细胞的增殖、侵袭和迁移。这些结果表明,miR-219 通过靶向 CD164 抑制髓母细胞瘤细胞的增殖、迁移和侵袭。结果还表明,miR-219 可能作为髓母细胞瘤的一种潜在治疗剂。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验