Zhang JW, Huang LY, Li YN, Tian Y, Yu J, Wang XF. Mitochondrial carrier homolog 2 increases malignant phenotype of human gastric epithelial cells and promotes proliferation, invasion, and migration of gastric cancer cells. World J Gastrointest Oncol 2024; 16(3): 991-1005 [PMID: 38577443 DOI: 10.4251/wjgo.v16.i3.991]
Corresponding Author of This Article
Jing-Wen Zhang, MD, Associate Professor, School of Basic Medical Science, NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, No. 1160 Shengli Street, Xingqing District, Yinchuan 750004, Ningxia Hui Autonomous Region, China. ztjwjwzt@163.com
Research Domain of This Article
Oncology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastrointest Oncol. Mar 15, 2024; 16(3): 991-1005 Published online Mar 15, 2024. doi: 10.4251/wjgo.v16.i3.991
Mitochondrial carrier homolog 2 increases malignant phenotype of human gastric epithelial cells and promotes proliferation, invasion, and migration of gastric cancer cells
Jing-Wen Zhang, Ya-Ning Li, Jia Yu, School of Basic Medical Science, NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
Ling-Yan Huang, Department of Pathology, General Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
Ying Tian, School of Clinical Medicine, Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
Xiao-Fei Wang, Department of Pathology, North China University of Science and Technology Affiliated Hospital, Tangshan 063000, Hebei Province, China
Author contributions: Zhang JW and Wang XF designed the research study; Yu J, Zhang JW, Tian Y, and Li YN performed the research; Huang LY, Li YN, and Tian Y analyzed the data; Huang LY, Wang XF, and Yu J wrote the manuscript; all authors have read and approve the final manuscript.
Supported bythe Medical Science Research Projects in Hebei Province, No. 20221526; and Natural Science Foundation, No. 2022-271.
Institutional review board statement: The study was reviewed and approved by the North China University of Science and Technology Institutional Review Board (Approval No. 2022032).
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Data sharing statement: Technical appendix, statistical code, and dataset available from the corresponding author at ztjwjwzt@163.com.
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: Jing-Wen Zhang, MD, Associate Professor, School of Basic Medical Science, NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, No. 1160 Shengli Street, Xingqing District, Yinchuan 750004, Ningxia Hui Autonomous Region, China. ztjwjwzt@163.com
Received: October 20, 2023 Peer-review started: October 20, 2023 First decision: December 5, 2023 Revised: December 21, 2023 Accepted: January 19, 2024 Article in press: January 19, 2024 Published online: March 15, 2024 Processing time: 144 Days and 6.4 Hours
Abstract
BACKGROUND
The precise role of mitochondrial carrier homolog 2 (MTCH2) in promoting malignancy in gastric mucosal cells and its involvement in gastric cancer cell metastasis have not been fully elucidated.
AIM
To determine the role of MTCH2 in gastric cancer.
METHODS
We collected 65 samples of poorly differentiated gastric cancer tissue and adjacent tissues, constructed MTCH2-overexpressing and MTCH2-knockdown cell models, and evaluated the proliferation, migration, and invasion of human gastric epithelial cells (GES-1) and human gastric cancer cells (AGS) cells. The mitochondrial membrane potential (MMP), mitochondrial permeability transformation pore (mPTP) and ATP fluorescence probe were used to detect mitochondrial function. Mitochondrial function and ATP synthase protein levels were detected via Western blotting.
RESULTS
The expression of MTCH2 and ATP2A2 in gastric cancer tissues was significantly greater than that in adjacent tissues. Overexpression of MTCH2 promoted colony formation, invasion, migration, MMP expression and ATP production in GES-1 and AGS cells while upregulating ATP2A2 expression and inhibiting cell apoptosis; knockdown of MTCH2 had the opposite effect, promoting overactivation of the mPTP and promoting apoptosis.
CONCLUSION
MTCH2 can increase the malignant phenotype of GES-1 cells and promote the proliferation, invasion, and migration of gastric cancer cells by regulating mitochondrial function, providing a basis for targeted therapy for gastric cancer cells.
Core Tip: Mitochondrial carrier homolog 2 (MTCH2) increases malignant phenotype of human gastric epithelial cells. MTCH2 promotes progression of gastric cancer cells. Mitochondrial permeability transformation pore opening and ATP synthase play important roles in gastric cancer.
