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LINC02163 通过 miR-593-3p/FOXK1 轴调控胃癌细胞的生长和上皮间质转化表型。

LINC02163 regulates growth and epithelial-to-mesenchymal transition phenotype via miR-593-3p/FOXK1 axis in gastric cancer cells.

机构信息

a Department of Gastroenterology , The First Affiliated Hospital of Wenzhou Medical University , Wenzhou City , China.

b Department of Anesthesiology , The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , Zhejiang , P.R. China.

出版信息

Artif Cells Nanomed Biotechnol. 2018;46(sup2):607-615. doi: 10.1080/21691401.2018.1464462. Epub 2018 Jun 12.

DOI:10.1080/21691401.2018.1464462
PMID:29893595
Abstract

Recently, long non-coding RNAs (lncRNAs) were involved in promoting gastric cancer (GC) initiation and progression. In the current study, we revealed that the expression level of LINC02163 was elevated in GC cell lines and tissues. Knockdown of LINC02163 inhibited GC cells growth and invasion both in vitro and in vivo. Mechanismly, LINC02163 exerted as a ceRNA and negatively regulated miR-593-3p expression. In addition, FOXK1 was identified as a down-stream target of miR-593-3p. The miR-593-3p/FOXK1 axis mediated LINC02163's effect on GC. To the best of our knowledge, our findings provided the first evidence that LINC02163 functioned as an oncogene in GC. LINC02163 may be a candidate prognostic biomarker and a target for new therapies in GC patients.

摘要

最近,长链非编码 RNA(lncRNA)被涉及促进胃癌(GC)的发生和发展。在本研究中,我们揭示了 LINC02163 的表达水平在 GC 细胞系和组织中升高。LINC02163 的敲低抑制了 GC 细胞在体外和体内的生长和侵袭。机制上,LINC02163 作为 ceRNA 并负调控 miR-593-3p 的表达。此外,FOXK1 被鉴定为 miR-593-3p 的下游靶标。miR-593-3p/FOXK1 轴介导 LINC02163 对 GC 的影响。据我们所知,我们的研究结果首次提供了证据表明 LINC02163 在 GC 中作为癌基因发挥作用。LINC02163 可能是 GC 患者的候选预后生物标志物和新治疗靶点。

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