Basic Study
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Nov 15, 2022; 14(11): 2170-2182
Published online Nov 15, 2022. doi: 10.4251/wjgo.v14.i11.2170
MiR-30e-3p inhibits gastric cancer development by negatively regulating THO complex 2 and PI3K/AKT/mTOR signaling
Xiao-Jing Gu, Ya-Jun Li, Fang Wang, Ting Ye
Xiao-Jing Gu, Ya-Jun Li, Fang Wang, Ting Ye, Department of Gastroenterology, General Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Prefecture, China
Author contributions: Gu XJ and Li YJ conceived, designed the experiments, wrote and revised the manuscript; Gu XJ, Li YJ, Wang F and Ye T performed the experiments; Wang F and Ye T analyzed and interpreted the data; All the authors have read and approved the final version of the manuscript.
Supported by National Natural Science Foundation of China, No. 81860442; and Ningxia Natural Science Foundation Project, No. 2022AAC03525.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board of Ningxia Medical University.
Institutional animal care and use committee statement: All animal experiments conformed to the internationally accepted principles for the care and use of laboratory animals.
Conflict-of-interest statement: The authors declare that they have no competing interests.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ya-Jun Li, Doctor, DPhil, Chief Doctor, Department of Gastroenterology, General Hospital of Ningxia Medical University, No. 804 Shengli South Street, Xingqing District, Yinchuan 750004, Ningxia Hui Autonomous Prefecture, China. lyajundoc@126.com
Received: July 15, 2022
Peer-review started: July 15, 2022
First decision: August 8, 2022
Revised: September 5, 2022
Accepted: October 12, 2022
Article in press: October 12, 2022
Published online: November 15, 2022
Processing time: 123 Days and 0.6 Hours
ARTICLE HIGHLIGHTS
Research background

Gastric cancer (GC) is a common type of digestive cancer with high morbidity and mortality rates worldwide.

Research motivation

Considerable effort has been expended in understanding the mechanism of GC development and metastasis.

Research objectives

We explored the expression and function of miR-30e-3p in GC development.

Research methods

We conducted quantitative real-time polymerase chain reaction, transfection, cell growth assays, transwell assay, luciferase reporter assay, western blot assays to explore the expression and function of miR-30e-3p.

Research results

Our findings revealed that knockdown of THO complex 2 (THOC2) inhibited the growth and metastatic behaviors of GC cells. After investigating signaling pathways involved in miR-30e-3p regulation, we found that the miR-30e-3p/THOC2 axis regulated the PI3K/AKT/mTOR pathway in GC.

Research conclusions

Our findings suggested that miR-30e-3p directly targets THOC2 and that THOC2 mediates the tumor suppression function of miR-30e-3p in GC. Low expression of miR-30e-3p or upregulation of THOC2 predicts poor prognosis of patients with GC. The diagnostic and therapeutic value of miR-30e-3p/THOC2 in GC should be further investigated in future studies.

Research perspectives

Considerable effort has been expended in understanding the mechanism of GC development and metastasis. Given that microRNAs have been found to participate in the regulation of GC progression.