GASTROENTEROLOGY / EXPERIMENTAL RESEARCH
TUG1 acts as a biomarker to predict the relapse of gastric cancer after endoscopic submucosal dissection
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Department of Gastroenterology, The First People’s Hospital of Yancheng, Yancheng, Jiangsu, China
Submission date: 2019-07-30
Final revision date: 2020-01-30
Acceptance date: 2020-03-11
Online publication date: 2021-03-28
Corresponding author
Yanping Hao
Department of Gastroenterology, The First People’s Hospital of Yancheng, No.66 Renmin Road, Yancheng, Jiangsu 224005, China
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ABSTRACT
Introduction:
MiR-382 was reported to act as a prognostic biomarker for the relapse of gastric cancer (GC) after endoscopic mucosal resection (EMR). In addition, TUG1 was reported to regulate cell proliferation via sponging miR-382. Therefore, in this study, we aimed to investigate the value of TUG1 in predicting post-EMR relapse of GC.
Material and methods:
The log rank test was utilized to analyze relapse-free rate and validate the prognostic value of TUG1 in predicting post-EMR GC relapse. Real-time PCR, Western blot and luciferase assays were performed to clarify the regulatory relationships among TUG1, miR-382 and CD44, thus establishing a TUG1/miR-382/CD44 signaling pathway. Moreover, MTT assays were conducted to observe the effect of TUG1 on cell proliferation and post-EMR GC relapse.
Results:
The AUC of the high TUG1 expression group was obviously smaller than that of the low TUG1 expression group, which indicated that the expression of TUG1 could be used as a prognostic biomarker to predict the risk of post-EMR GC relapse. In addition, a negative correlation was found between miR-382 expression and the expression of its endogenous competing RNA TUG1. Furthermore, miR-382 was shown to inhibit the expression of its target gene CD44. Finally, a TUG1/miR-382/CD44 signaling pathway was established and was implicated in post-EMR recurrence of GC, and the overexpression of TUG1 was shown to promote the proliferation of GC cells.
Conclusions:
Reduced expression of TUG1 could inhibit the proliferation of GC cells and increase the expression of miR-382, which in turn down-regulated CD44 expression and lowered the risk of post-EMR GC relapse.