miR-223 regulates migration and invasion by targeting Artemin in human esophageal carcinoma.
miR-223 regulates migration and invasion by targeting Artemin in human esophageal carcinoma.
复制标题
miR-223通过靶向Artemin调节人食管癌的迁移和侵袭
DOI：
10.1186/1423-0127-18-24
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发表时间：
2011-03-31
影响因子：
11
通讯作者：
Zhou Q
中科院分区：
文献类型：
--
作者：
Li S;Li Z;Guo F;Qin X;Liu B;Lei Z;Song Z;Sun L;Zhang HT;You J;Zhou Q
Artemin（ARTN）是一种神经营养因子，属于神经胶质细胞源性神经营养因子配体家族。方法采用Western blot方法检测食管癌细胞系KYSE-150、KYSE-510、EC-9706、TE 13、食管癌组织及配对癌旁组织中ARTN的表达水平。构建Artemin siRNA表达载体以敲低artemin表达减轻KYSE 150细胞中的迁移和侵袭。采用单层伤口愈合实验和Transwell侵袭实验观察癌细胞的迁移和侵袭能力。RTN的相对表达水平通过实时定量PCR进行定量。结果ARTN在食管癌组织中的表达水平高于癌旁组织，且在各种食管癌细胞系中差异表达。ARTN mRNA在3 'UTR中含有miR-223的结合位点。在双荧光素酶报告基因分析中，将mir-223表达载体与pMIR-ARTN共转染导致荧光素酶活性降低，表明ARTN是miR-223的靶基因。miR-223过表达降低KYSE 150细胞中ARTN的表达，而沉默miR-223增加EC 9706细胞中ARTN的表达。此外，miR-223在KYSE 150细胞中的过表达降低了细胞的迁移和侵袭。EC 9706细胞中miR-223的沉默增加了细胞的迁移和侵袭力。结论这些结果表明，ARTN，一个已知的肿瘤转移相关基因，是miR-223的直接靶点，miR-223可能在食管癌中具有肿瘤抑制功能，并可用于抗癌治疗。
BackgroundArtemin (ARTN) is a neurotrophic factor belonging to the glial cell-derived neurotrophic factor family of ligands. To develop potential therapy targeting ARTN, we studied the roles of miR-223 in the migration and invasion of human esophageal carcinoma.MethodsARTN expression levels were detected in esophageal carcinoma cell lines KYSE-150, KYSE-510, EC-9706, TE13, esophageal cancer tissues and paired non-cancerous tissues by Western blot. Artemin siRNA expression vectors were constructed to knockdown of artemin expression mitigated migration and invasiveness in KYSE150 cells. Monolayer wound healing assay and Transwell invasion assay were applied to observe cancer cell migration and invasion. The relative levels of expression were quantified by real-time quantitative PCR.ResultsARTN expression levels were higher in esophageal carcinoma tissue than in the adjacent tissue and was differentially expressed in various esophageal carcinoma cell lines. ARTN mRNA contains a binding site for miR-223 in the 3'UTR. Co-transfection of a mir-223 expression vector with pMIR-ARTN led to the reduced activity of luciferase in a dual-luciferase reporter gene assay, suggesting that ARTN is a target gene of miR-223. Overexpression of miR-223 decreased expression of ARTN in KYSE150 cells while silencing miR-223 increased expression of ARTN in EC9706 cells. Furthermore, overexpression of miR-223 in KYSE150 cells decreased cell migration and invasion. Silencing of miR-223 in EC9706 cells increased cell migration and invasiveness.ConclusionsThese results reveal that ARTN, a known tumor metastasis-related gene, is a direct target of miR-223 and that miR-223 may have a tumor suppressor function in esophageal carcinoma and could be used in anticancer therapies.
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影响因子：
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作者：
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通讯作者：
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