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Enhanced Succinate Oxidation with Mitochondrial Complex II Reactive Oxygen Species Generation in Human Prostate
Aijun Zhang1,2, Anisha A Gupte1,2, Somik Chatterjee1
1Center for Bioenergetics, Houston Methodist Research Institute, Houston, TX 77030, USA.
International Journal of Molecular Sciences
|October 27, 2022
Summary
Prostate cancer (PCa) cells show altered mitochondrial respiration, favoring Complex II (CII) over Complex I (CI). This suggests succinate and CII are potential therapeutic targets for PCa.
Area of Science:
- Biochemistry
- Oncology
- Mitochondrial Biology
Background:
- Prostate cancer (PCa) involves a metabolic shift from citrate secretion to oxidation.
- This transition is linked to decreased mitochondrial zinc and altered respiratory flux.
- Previous studies relied on indirect evidence from models and preserved tissues.
Purpose of the Study:
- To analyze mitochondrial Complex I (CI) and Complex II (CII) electron flow in fresh human PCa tissue.
- To identify alterations in the electron transport system (ETS) in malignant prostate tissue.
Main Methods:
- Direct respiratory analysis of fresh human prostate tissue.
- Assessment of mitochondrial CI and CII activity.
- Evaluation of electron flow to the Q-junction.
Main Results:
- Fresh non-malignant prostate tissue exhibits a Complex II (CII) succinate: quinone oxidoreductase (SQR) dominant oxidative flux.
- This CII-driven flux is enhanced in malignant prostate tissue.
- Complex I (CI) NADH: ubiquinone oxidoreductase activity is impaired in high-grade PCa.
Conclusions:
- Prostate cancer exhibits a shift towards CII-dominant respiration.
- Succinate and CII represent promising therapeutic targets for PCa treatment and prevention.
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