Published online Mar 15, 2024. doi: 10.4251/wjgo.v16.i3.991
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
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.
To determine the role of MTCH2 in gastric cancer.
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 mito
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.
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.