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

被引：30

作者：

Dong, Lemei ^{[1
]}

Hong, Huisuo ^{[2
]}

Chen, Xiaowei ^{[1
]}

Huang, Zhiming ^{[1
]}

Wu, Wei ^{[1
]}

Wu, Fang ^{[1
]}

机构：

[1] Wenzhou Med Univ, Dept Gastroenterol, Affiliated Hosp 1, Wenzhou City, Peoples R China

[2] Wenzhou Med Univ, Dept Anesthesiol, Affiliated Hosp 1, Wenzhou, Zhejiang, Peoples R China

来源：

ARTIFICIAL CELLS NANOMEDICINE AND BIOTECHNOLOGY | 2018年 / 46卷

关键词：

LINC02163; miR-593-3p; FOXK1; gastric cancer; PROLIFERATION; METASTASIS; CERNA; CONTRIBUTES; CARCINOMA; APOPTOSIS; INVASION; SPONGE; FOXK1;

D O I：

10.1080/21691401.2018.1464462

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

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.

引用

页码：607 / 615

页数：9

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