TUG1 acts as a biomarker to predict the relapse of gastric cancer after endoscopic submucosal dissection.

[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.