miR-532 promoted gastric cancer migration and invasion by targeting NKD1

被引：63

作者：

Hu, Shaobo ^{[1
]}

Zheng, Qichang ^{[1
]}

Wu, Heshui ^{[2
]}

Wang, Chunyou ^{[2
]}

Liu, Tao ^{[2
]}

Zhou, Wei ^{[2
]}

机构：

[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Dept Hepatobiliary Surg, Wuhan 430022, Hubei Province, Peoples R China

[2] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Dept Pancreat Surg, 1277 Jiefang Ave, Wuhan 430022, Hubei Province, Peoples R China

来源：

LIFE SCIENCES | 2017年 / 177卷

关键词：

miR-532; Gastric cancer; NKD1; Migration; Invasion; DOWN-REGULATION;

D O I：

10.1016/j.lfs.2017.03.019

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Gastric cancer is one of the most common human malignant neoplasms, especially in China, its regulatory mechanismis important to develop new therapy approaches. miRNAs have been demonstrated to regulate gastric cancer progression. We found miR-532 was overexpressed in gastric cancer tissues and cells. Wound healing and transwell assay revealed that its overexpression promoted gastric cancer cell migration and invasion, its knockdown inhibited gastric cancer cell migration and invasion. Wnt/beta-catenin antagonist naked cuticle homolog 1 (NKD1) was the target of miR-532, miR-532 inhibited NKD1 expression. TOP/FOP luciferase activity analysis suggested miR-532 also increased Wnt/beta-catenin pathway activity. Overexpression miR-532 and NKD1 inhibited gastric cancer cell migration and invasion, consistent with miR-532 knockdown. These findings revealed miR-532 promoted gastric cancer cell migration and invasion through inhibiting NKD1 and activated Wnt/beta-catenin pathway. We provide a potential target for gastric cancer therapy. (C) 2017 Published by Elsevier Inc.

引用

页码：15 / 19

页数：5

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