首页> 外文期刊>European Journal of Cell Biology: Journal of Deutsche Gesellschaft fur Elektronenmikroskopie: Journal of Deutsche Gesellschaft fur Zellbiologie >CXCR4 3 ' UTR functions as a ceRNA in promoting metastasis, proliferation and survival of MCF-7 cells by regulating miR-146a activity
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CXCR4 3 ' UTR functions as a ceRNA in promoting metastasis, proliferation and survival of MCF-7 cells by regulating miR-146a activity

机译:CXCR4 3'UTR通过调节miR-146a活性作为ceRNA促进MCF-7细胞的转移,增殖和存活

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摘要

CXCR4 is the most common chemokine receptor expressed on tumor cells, and it is closely correlated with cancer cell sternness. This study was carried out to explore whether CXCR4 could function as a competitive endogenous RNA to promote metastasis, proliferation and survival in MCF-7 breast cancer cells. We validated that CXCR4, together with TRAF6 and EGFR, was directly targeted by miR-146a in MCF-7 cells. Overexpression of CXCR4 3'UTR inhibited the activity of miR-146a, thus elevating the expression of CXCR4, TRAF6 and EGFR. These oncoproteins further activated NF-KB pathway and promoted the proliferation, migration, invasion and anti-apoptotic activity of MCF-7 cells. Collectively, our study provided new insights into the function of CXCR4 in breast cancer: it promotes tumor progression as both a protein-coding gene and a non-coding RNA, complicating the mechanism by which oncogenes promote tumor progression. (C) 2015 Elsevier GmbH. All rights reserved.
机译:CXCR4是在肿瘤细胞上表达的最常见的趋化因子受体,它与癌细胞的严厉性密切相关。进行这项研究以探讨CXCR4是否可以作为竞争性内源RNA来促进MCF-7乳腺癌细胞的转移,增殖和存活。我们验证了miR-146a在MCF-7细胞中直接靶向CXCR4,TRAF6和EGFR。 CXCR4 3'UTR的过表达抑制了miR-146a的活性,从而提高了CXCR4,TRAF6和EGFR的表达。这些癌蛋白进一步激活了NF-KB通路,并促进了MCF-7细胞的增殖,迁移,侵袭和抗凋亡活性。总的来说,我们的研究为CXCR4在乳腺癌中的功能提供了新的见解:它既作为蛋白质编码基因又作为非编码RNA促进肿瘤进展,使致癌基因促进肿瘤进展的机制变得复杂。 (C)2015 Elsevier GmbH。版权所有。

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