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Erschienen in: Gastric Cancer 2/2019

01.03.2019 | Original Article

Downregulation of miR-142-5p promotes tumor metastasis through directly regulating CYR61 expression in gastric cancer

verfasst von: Jing Yan, Bing Yang, Shuye Lin, Rui Xing, Youyong Lu

Erschienen in: Gastric Cancer | Ausgabe 2/2019

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Abstract

Background

Recurrence is a primary cause of gastric cancer (GC)-related deaths. We reported previously that low expression of miR-142-5p could predict recurrence in GC. The present study aimed to investigate the function and mechanism of miR-142-5p in metastasis of GC.

Methods

MiR-142-5p expression was detected in 101 GC samples by qRT-PCR. Its clinical significance was statistically analyzed. The roles of miR-142-5p and its candidate target gene CYR61 in metastasis were determined both in vivo and in vitro.

Results

MiR-142-5p downregulation was significantly associated with the recurrence (P = 0.031) and poor prognosis of GC (P = 0.043). MiR-142-5p inhibited cancer cell migration and invasion both in vitro and in vivo. CYR61 was identified as a novel direct target of miR-142-5p by bioinformatics analysis of target prediction and luciferase reporter assay. The re-expression and knockdown of CYR61 could, respectively, rescue the effects induced by miR-142-5p overexpression and knockdown. MiR-142-5p attenuated GC cell migration and invasion, at least partially, by inactivation of the canonical Wnt/β-catenin signaling pathway through CYR61.

Conclusions

The newly identified miR-142-5p-CYR61-Wnt/β-catenin axis partially illustrates the molecular mechanism of GC recurrence and represents a novel prognosis biomarker for GC.
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Metadaten
Titel
Downregulation of miR-142-5p promotes tumor metastasis through directly regulating CYR61 expression in gastric cancer
verfasst von
Jing Yan
Bing Yang
Shuye Lin
Rui Xing
Youyong Lu
Publikationsdatum
01.03.2019
Verlag
Springer Singapore
Erschienen in
Gastric Cancer / Ausgabe 2/2019
Print ISSN: 1436-3291
Elektronische ISSN: 1436-3305
DOI
https://doi.org/10.1007/s10120-018-0872-4

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