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Related Concept Videos

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

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Related Experiment Video

Updated: Jun 13, 2026

Assessment of Mitochondrial Health in Cancer-Associated Fibroblasts Isolated from 3D Multicellular Lung Tumor Spheroids
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Mitochondrial Metabolic Reprogramming in Colorectal Cancer-Associated Fibroblasts: An Up-to-Date Review.

Ying Li1,2, Dipanjan Chanda3, Seong-Woo Jeon4

  • 1BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University, Daegu 41944, Republic of Korea.

Cancers
|June 12, 2026
PubMed
Summary
This summary is machine-generated.

Cancer-associated fibroblasts (CAFs) reprogram their mitochondria, driving colorectal cancer (CRC) growth and treatment resistance. Targeting CAF mitochondria offers a new strategy to disrupt tumor-stroma metabolic cooperation in CRC.

Keywords:
cancer-associated fibroblastscolorectal cancermetabolic reprogrammingmitochondriatumor microenvironment

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Area of Science:

  • Oncology
  • Cancer Metabolism
  • Tumor Microenvironment

Background:

  • Colorectal cancer (CRC) progression involves metabolic interactions between tumor cells and the tumor microenvironment (TME).
  • Cancer-associated fibroblasts (CAFs) within the TME are key metabolic drivers, influencing tumor growth, therapeutic resistance, and immune evasion.
  • Mitochondrial reprogramming in CAFs plays a critical role in CRC biology.

Purpose of the Study:

  • To review current understanding of how CAF mitochondrial dynamics and metabolic reprogramming influence colorectal cancer.
  • To explore the functional diversity of CAFs and their specific mitochondrial needs.
  • To identify CAF mitochondria as a potential therapeutic target in CRC.

Main Methods:

  • Literature review synthesizing recent research on CAF mitochondrial function in CRC.
  • Analysis of CAF subpopulations and their mitochondrial requirements.
  • Evaluation of regulatory pathways governing CAF mitochondrial reprogramming and metabolic symbiosis.

Main Results:

  • CAF mitochondrial reprogramming significantly impacts CRC growth, resistance, and immune evasion.
  • Tumor-derived signals modulate stromal mitochondrial function, creating metabolic symbiosis via nutrient shuttling (lactate, ketone, glutamine).
  • Remodeled CAF mitochondria contribute to redox homeostasis and immunosuppression, driving resistance to various cancer therapies.

Conclusions:

  • CAF mitochondria are central to tumor-stroma metabolic cooperation and treatment resistance in CRC.
  • Targeting CAF-specific mitochondrial pathways presents a novel strategy to overcome therapeutic resistance.
  • Understanding CAF mitochondrial metabolism is crucial for developing effective CRC treatments.