LncRNA RP11-436H11.5, functioning as a competitive endogenous RNA, upregulates BCL-W expression by sponging miR-335-5p and promotes proliferation and invasion in renal cell carcinoma.
LncRNA RP11-436H11.5, functioning as a competitive endogenous RNA, upregulates BCL-W expression by sponging miR-335-5p and promotes proliferation and invasion in renal cell carcinoma.
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LncRNA RP11-436H11.5作为竞争性内源RNA，通过海绵miR-335-5p上调BCL-W表达并促进肾细胞癌的增殖和侵袭
DOI：
10.1186/s12943-017-0735-3
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发表时间：
2017-10-25
期刊：
影响因子：
37.3
通讯作者：
Fei X
中科院分区：
文献类型：
--
作者：
Wang K;Jin W;Song Y;Fei X
越来越多的证据表明，长链非编码RNA（lncRNA）在肿瘤发生中起着至关重要的作用。在这里，我们报告了一种新的lncRNA，RP 11 - 436 H11.5，它通过海绵状miR-335- 5 p调节肾细胞癌（RCC）细胞的增殖和侵袭。通过qRT-PCR测定法测定RCC组织中lncRNA RP 11 - 436 H11.5的表达。通过细胞增殖测定和transwell侵袭测定来测量RCC细胞增殖和侵袭。Western blot检测BCL-W的表达。通过荧光素酶报告基因测定和RNA下拉测定测量lncRNA RP 11 - 436 H11.5和miR-335- 5 p之间的相互作用。体内实验用于检测肿瘤形成。在本研究中，qRT-PCR结果表明lncRNA RP 11 -436H11.5在RCC组织中比在邻近正常肾组织中更高表达。生存分析结果表明，高lncRNA RP 11 - 436 H11.5组患者的预后明显差于低lncRNA RP 11 - 436 H11.5组。lncRNA RP 11 -436H11.5的下调在体外和体内抑制RCC细胞的增殖和侵袭。荧光素酶报告基因分析结果表明，lncRNA RP 11 - 436 H11.5通过调节miR-335- 5 p表达增强BCL-W表达。LncRNA RP 11 -436H11.5可作为miR-335- 5 p诱饵发挥下调BCL-W表达的作用。LncRNA RP 11 -436H11.5可作为竞争性内源性RNA促进RCC细胞增殖和侵袭，这可能作为抑制RCC进展的治疗应用。
Accumulating evidence indicates that long non-coding RNAs (lncRNAs) play a crucial role in tumorigenesis. Here, we report a novel lncRNA, RP11-436H11.5, that regulates renal cell carcinoma (RCC) cell proliferation and invasion by sponging miR-335-5p. Expression of lncRNA RP11-436H11.5 was determined by a qRT-PCR assay in RCC tissues. RCC cell proliferation and invasion were measured by a cell proliferation assay and a transwell invasion assay. Expression of BCL-W was detected by a western blot assay. Interactions between lncRNA RP11-436H11.5 and miR-335-5p were measured by a luciferase reporter assay and a RNA-pull down assay. In vivo experiments were used to detect tumor formation. In this study, the qRT-PCR results illustrated that lncRNA RP11-436H11.5 was more highly expressed in RCC tissues than in adjacent normal renal tissues. The results of survival analysis indicated that patients in the high lncRNA RP11-436H11.5 group presented significantly worse outcomes compared with those in the low lncRNA RP11-436H11.5 group. Downregulation of lncRNA RP11-436H11.5 suppressed RCC cell proliferation and invasion in vitro and in vivo. Luciferase reporter assay results demonstrated that lncRNA RP11-436H11.5 enhanced BCL-W expression by regulating miR-335-5p expression. LncRNA RP11-436H11.5 could function as a miR-335-5p decoy to derepress expression of BCL-W. LncRNA RP11-436H11.5 could function as a competing endogenous RNA to promote RCC cell proliferation and invasion, which might serve as a therapeutic application to suppress RCC progression.
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