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Circular RNA circFGD4 suppresses gastric cancer progression via modulating miR-532-3p/APC/β-catenin signalling pathway.

Authors :
Xinglong Dai
Jianjun Liu
Xiong Guo
Anqi Cheng
Xiaoya Deng
Liqun Guo
Ziwei Wang
Source :
Clinical Science; Jul2020, Vol. 134 Issue 13, p1821-1839, 19p
Publication Year :
2020

Abstract

Background: Mounting evidence has displayed critical roles of circular RNAs (circRNAs) in multiple cancers. The underlying mechanisms by which circFGD4 contributed to gastric cancer (GC) are still unclear. Methods: The levels and clinical values of circFGD4 in GC patients were detected and analysed by quantitative real-time PCR. The biological roles of circFGD4 in GC were assessed in vitro and in vivo experiments. Dual-luciferase reporter, fluorescence in situ hybridization, RNA immunoprecipitation, biotin-coupled RNA pull-down, and TOP/Flash and FOP/Flash reporter gene assays were employed to evaluate the effects of circFGD4 on miR-532-3p-mediated adenomatous polyposis coli (APC)/β-catenin signalling in GC cells. Results: circFGD4 expression was down-regulated the most in human GC tissues and cell lines. Low expression of circFGD4 was correlated with poor tumour differentiation, lymphatic metastasis, and poor prognosis of GC patients. circFGD4 suppressed GC cell viability, colony formation, migration, induced epithelial-mesenchymal transition (EMT), and tumorigenesis and metastasis in vivo. Next, we validated that circFGD4 acted as a sponge of miR-532-3p to relieve the tumour-promoting effects of miR-532-3p on its target APC. The mechanistic analysis demonstrated that the circFGD4 suppressed GC cell viability, migration, and EMT bymodulating the miR-532-3p/APC axis to inactivate the ß-catenin signalling. Conclusion: circFGD4 suppressed GC progression through sponging miR-532-3p and enhancing APC expression to inactivate the ß-catenin signalling. Thus circFGD4 provides a novel potential biomarker and valuable therapeutic strategy for GC. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
01435221
Volume :
134
Issue :
13
Database :
Complementary Index
Journal :
Clinical Science
Publication Type :
Academic Journal
Accession number :
144819341
Full Text :
https://doi.org/10.1042/CS20191043