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Updated: May 9, 2026
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Transmitochondrial Cybrid Generation Using Cancer Cell Lines
Published on: March 17, 2023
Proteomic and Metabolomic Profiling Reveal Mitochondrial Transplantation-Mediated Reprogramming in Gastric Cancer
Ping-Chen Chen1, Chen-Kai Liu2, Ching-Chung Tsai3,4
1Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan.
The Kaohsiung Journal of Medical Sciences
|May 8, 2026
Summary
Transplanted gastric epithelial cell mitochondria (GES-1) were found to reduce gastric cancer cell (AGS) malignancy by altering cellular metabolism. This study reveals how mitochondrial transplantation impacts pyruvate accumulation and inhibits cancer cell migration.
Area of Science:
- Cell Biology
- Mitochondrial Biology
- Cancer Research
Background:
- Mitochondria are crucial for cellular functions.
- Previous studies showed GES-1 mitochondria reduce AGS gastric cancer malignancy.
- The underlying mechanisms require elucidation.
Purpose of the Study:
- To investigate the molecular mechanisms by which transplanted GES-1 mitochondria attenuate AGS gastric cancer malignancy.
- To analyze proteomic and metabolomic changes induced by mitochondrial transplantation.
Main Methods:
- TMT-based proteomic analysis and Ingenuity Pathway Analysis.
- Western blotting for protein verification.
- Metabolomic analysis of glycolysis, TCA cycle, pentose phosphate pathway (PPP), and ATP production.
- Pyruvate and lactate assays.
Main Results:
- Proteomic analysis identified 257 upregulated and 34 downregulated proteins in 14 signaling pathways, including mitochondrial dysfunction.
- Metabolomic analysis revealed altered metabolites in glycolysis, TCA cycle, PPP, and ATP production, suggesting pyruvate accumulation.
- Transplanted mitochondria led to increased pyruvate, decreased extracellular lactate, and inhibited AGS cell migration.
Conclusions:
- Transplanted GES-1 mitochondria attenuate AGS gastric cancer malignancy.
- Mechanisms involve altered cellular metabolism, pyruvate accumulation, and subsequent inhibition of cancer cell migration.
