Open Access

ARTICLE

miR-216a-3p Inhibits the Proliferation, Migration, and Invasion of Human Gastric Cancer Cells via Targeting RUNX1 and Activating the NF-κB Signaling Pathway

Yinfang Wu^*, Jun Zhang^†, Yu Zheng^‡, Cheng Ma^‡, Xing-E Liu^§, Xiaodong Sun^*‡

* The Second Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province, P.R. China
† Department of Gastroenterology, Zhejiang Provincial People’s Hospital, Hangzhou, Zhejiang Province, P.R. China
‡ Department of Hepatobiliary and Pancreatic Surgery, Zhejiang Provincial People’s Hospital, Hangzhou, Zhejiang Province, P.R. China
§ Department of Medical Oncology, Zhejiang Hospital, Hangzhou, Zhejiang Province, P.R. China

Oncology Research 2018, 26(1), 157-171. https://doi.org/10.3727/096504017X15031557924150

Abstract

This work aims to elucidate the effects and the potential underlying mechanisms of microRNA-216a-3p (miR- 216a-3p) on the proliferation, migration, and invasion of gastric cancer (GC) cells. In this study, we revealed that the expression of miR-216a-3p was significantly elevated in GC tissues and cell lines. The different expression level of miR-216a-3p was firmly correlated with clinicopathological characteristics of GC patients. We next demonstrated that upregulation of miR-216a-3p could dramatically promote the ability of proliferation, migration, and invasion of GC cells using a series of experiments, whereas downregulation essentially inhibited these properties. Additionally, through bioinformatics analysis and biological approaches, we confirmed that runt-related transcription factor 1 (RUNX1) was a direct target of miR-216a-3p, and overexpression of RUNX1 could reverse the potential effect of miR-216a-3p on GC cells. Furthermore, mechanistic investigation using Western blot analysis showed that downregulation of RUNX1 by miR-216a-3p could stimulate the activation of NF-kB signaling pathway. In summary, this work proved that miR-216a-3p can promote GC cell proliferation, migration, and invasion via targeting RUNX1 and activating the NF-kB signaling pathway. Therefore, miR-216a-3p/RUNX1 could be a possible molecular target for innovative therapeutic agents against GC.

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Keywords

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