Mitochondrial metabolism in cancer stem cells: a therapeutic target for colon cancer
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Updated: Apr 4, 2026
Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines
Published on: March 17, 2023
In-Sung Song1, Yu Jeong Jeong1, Jin Han1
1National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan 47392, Korea.
Abstract:
It has been proposed that the selective elimination of cancer stem cells (CSCs) using targeted therapy could greatly reduce tumor growth, recurrence, and metastasis. To develop effective therapeutic targets for CSC elimination, we aimed to define the properties of CSC mitochondria, and identify CSC-mitochondria- specific targets in colon cancer. We found that colon CSCs utilize mitochondrial oxidative phosphorylation (OXPHOS) to produce ATP. We also found that forkhead box protein 1 (FOXM1)-induced peroxiredoxin 3 (PRDX3) maintains the mitochondrial function, and the FOXM1/PRDX3 mitochondrial pathway maintains survival of colon CSCs. Furthermore, FOXM1 induces CD133 (PROM1/prominin 1) expression, which maintains the stemness of colon CSCs. Together, our findings indicate that FOXM1, PRDX3, and CD133 are potential therapeutic targets for the elimination of CSCs in colon cancer.
Insights
Targeting cancer stem cells (CSCs) is key to reducing colon cancer recurrence. Researchers identified the FOXM1/PRDX3 pathway and CD133 as crucial for CSC survival and stemness, offering new therapeutic targets.
Area of Science:
- Oncology
- Cell Biology
- Biochemistry
Background:
- Targeted elimination of cancer stem cells (CSCs) may reduce tumor growth, recurrence, and metastasis.
- Identifying CSC-specific targets is crucial for developing effective therapies.
Purpose of the Study:
- To define colon cancer CSC mitochondrial properties.
- To identify CSC-mitochondria-specific targets in colon cancer.
Main Methods:
- Analysis of colon CSC mitochondrial function.
- Investigation of the role of FOXM1, PRDX3, and CD133 in CSC survival and stemness.
Main Results:
- Colon CSCs rely on mitochondrial oxidative phosphorylation (OXPHOS) for ATP production.
- The FOXM1/PRDX3 pathway maintains mitochondrial function and colon CSC survival.
- FOXM1 induces CD133 expression, preserving colon CSC stemness.
Conclusions:
- FOXM1, PRDX3, and CD133 are critical for colon CSC survival and stemness.
- These molecules represent potential therapeutic targets for colon cancer elimination.
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