Down-regulation of miR-326 is associated with poor prognosis and promotes growth and metastasis by targeting FSCN1 in gastric cancer

Abstract

Background: MicroRNAs (miRNAs) have been documented as playing important roles in diverse biological processes including tumorigenesis. However, the function and mechanism of miR-326 in gastric cancer are still unknown. The aim of this study is to identify the role of miR-326 in gastric cancer and clarify the regulation of Fascin1 (FSCN1) by miR-326. Methods: The expression levels of miR-326 were detected in gastric cancer samples and cell lines by real-time PCR. The clinical and prognostic significance of miR-326 in gastric cancer patients were analyzed. Furthermore, the function of miR-326 on tumor cell growth and mobility were explored through MTT, colony formation, Transwell migration and invasion assays in vitro. A miR-326 target was confirmed using luciferase reporter assays, real-time PCR and Western blot. Results: Our study showed that miR-326 expression was decreased in gastric cancer tissues and cell lines, and low expression of miR-326 was associated to clinical stage, tumor depth, lymph node metastasis and distant metastasis. In survival analysis, low expression of miR-326 was a poor independent prognostic factor for gastric cancer patients. Gain-of-function and loss-of-function studies showed that miR-326 served as a tumor suppressor regulating gastric cancer cells growth, migration and invasion. Furthermore, we identified FSCN1 as the functional target of miR-326 by directly targeting the 3′-UTR of FSCN1. Conclusions: Our study demonstrated that miR-326 overexpression was a poor prognostic marker for gastric cancer patients, and miR-326 served as a tumor suppressor in gastric cancer via directly regulating FSCN1.

• FSCN1
• gastric cancer
• miR-326
• prognosis

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.

Supplementary material available online Supplementary Figure S1