What question did this study set out to answer?

To elucidate the mechanisms by which mitochondrial complex I defects enhance tumorigenesis and assess whether restoring oxidative phosphorylation or suppressing oxidative stress reverses tumor progression.

September 2, 2011Human Molecular GeneticsOpen Access

Mitochondrial respiratory complex I dysfunction promotes tumorigenesis through ROS alteration and AKT activation

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Authors

LSLokendra Kumar SharmaSanjay Gandhi Post Graduate Institute of Medical Sciences HFHezhi FangChinese Academy of Medical Sciences & Peking Union Medical College JLJiangtao LiuHarbin Medical University

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Implication

Preclinical study reveals that complex I dysfunction drives tumorigenesis through reactive oxygen species-dependent AKT activation in cancer cells, highlighting potential therapeutic targets.

Key Points

To elucidate the mechanisms by which mitochondrial complex I defects enhance tumorigenesis and assess whether restoring oxidative phosphorylation or suppressing oxidative stress reverses tumor progression.
Expressed yeast NADH quinone oxidoreductase (NDI1) in complex I-deficient cells harboring an ND5 subunit mutation to bypass the defective enzyme.
Suppressed complex I with rotenone or induced oxidative stress with paraquat, and treated cells with antioxidants to evaluate changes in AKT phosphorylation and tumorigenicity.
Expression of yeast NDI1 bypassed complex I defects, restored oxidative phosphorylation, and reversed the tumorigenic phenotype.
Suppression of complex I by rotenone or oxidative stress induction by paraquat increased AKT phosphorylation and enhanced tumorigenesis.
Antioxidant treatment suppressed reactive oxygen species-mediated AKT activation and reversed the tumorigenicity of complex I-deficient cells.

Cite This Study

Sharma et al. (2011) studied this question.

synapsesocial.com/papers/6a86b235a6ddb97d43d3b404 https://doi.org/10.1093/hmg/ddr395

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Implication

Preclinical study reveals that complex I dysfunction drives tumorigenesis through reactive oxygen species-dependent AKT activation in cancer cells, highlighting potential therapeutic targets.

Mitochondrial respiratory complex I dysfunction promotes tumorigenesis through ROS alteration and AKT activation

Discussion

Member takes

Implication

Key Points

Cite This Study

Mitochondrial respiratory complex I dysfunction promotes tumorigenesis through ROS alteration and AKT activation

Discussion

Member takes

Implication

Key Points

Cite This Study

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