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
Mitochondrial carrier homolog 2 (MTCH2), as an insertion enzyme of mitochondrial outer membrane protein, plays an important role in cellular production, energy expenditure and apoptosis induced by mitochondrial permeability transformation pore (mPTP) opening.
MTCH2 has been poorly studied in gastric cancer. The addition of MTCH2 research will provide a broader idea for the treatment of gastric cancer.
To investigate the precise role of MTCH2 in gastric cancer will providing a basis for the targeted therapy of gastric cancer.
Sixty-five samples of poorly differentiated gastric cancer tissue and adjacent tissues were collected for MTCH2 and ATP2A2 expression detection. JC-1, mPTP, and ATP fluorescence probe were used for mitochondrial function detection. Wound healing, transwell, and colony formation assay were used for cell migration and proliferation evaluation. Western blotting experiments were conducted to detect the changes in the expression levels of related proteins.
Both MTCH2 and ATP2A2 are highly expressed in gastric cancer. MTCH2 promotes proliferation and migration of gastric cancer cells, enhances mitochondrial activity, and inhibits apoptosis.
MTCH2 plays an important role in cellular production, energy expenditure and apoptosis in gastric cancer cells.
We speculate that the regulation of MTCH2 opening to mPTP may be related to the regulatory mechanism of calcium homeostasis, which will be further studied in the future.