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Updated: Sep 20, 2025

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Published on: October 27, 2020
CircRNA PVT1 modulated cell migration and invasion through Epithelial-Mesenchymal Transition (EMT) mediation in
Huanqin Li1, Shuai Xue1, Xiaohong Zhang1
1Endoscopy Center, Minhang Hospital, Fudan University, 170 Xin-Song Road, Shanghai 201199, PR China.
Background:
Gastric cancer (GC) progression is related with gene regulations.
Objectives:
This study explored underlying regulatory axis of circRNA PVT1 (circPVT1) in GC.
Methods:
GC cell lines were detected for circPVT1 expression with the normal mucous epithelial cell GES-1 as control. After regulation of circPVT1, miR-423-5p and SMAD3 expression through transfection, CCK8 evaluated the cell viability, Transwell measured the migratory and invasive capability of cells. Luciferase verified the paired bindings between miR-423-5p and CircPVT1 or SMAD3. The functions of CircPVT1/miR-423-5p/SMAD3 were evaluated using RT-PCR, CCK8, Transwell assays. Western blot analyzed EMT-related proteins and phosphorylation of Smad3 in GC cells. Immunofluorescence method was used to evaluate the EMT-related proteins as well.
Results:
CircPVT1 displayed higher expression in GC cells and knockdown led to decrease in cell growth, invasion and migration. CircPVT1 was targeted by miR-423-5p as a ceRNA of SMAD3. miR-423-5p upregulation suppressed both cicRNA PVT1 and SMAD3 in GC cells. Decrease in SMAD3 expression suppressed CircPVT1 by releasing miR-423-5p in cells, inhibiting cell growth, invasion and migration and suppressing the EMT process.
Conclusion:
CircPVT1 modulated cell growth, invasion and migration through EMT mediation in gastric cancer through miR-423-5p/Smad3 pathway.
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