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Updated: Mar 19, 2026

Author Spotlight: High-Throughput Measurement of Intracellular ROS Levels in Hepatocellular Lines
Published on: January 19, 2024
Reactive oxygen species: The good, the bad, and the enigma
1IFOM Foundation - FIRC Institute of Molecular Oncology Foundation ; Milan, Italy.
Abstract:
Work carried out primarily in the laboratory of Fabrizio d'Adda di Fagagna unveils the mitogenic properties of Ras-induced reactive oxygen species (ROS) and their relationship with the DNA damage response. Combined data from studies of cultured cells, zebrafish models, and clinical material consistently support a role of the RAS-RAC1-NOX4 axis in ROS induction, hyperproliferation, and senescence.
Insights
Ras proteins stimulate reactive oxygen species (ROS) production, promoting cell proliferation and DNA damage. The RAS-RAC1-NOX4 pathway is key to this process, impacting cell growth and aging.
Area of Science:
- Cellular Biology
- Molecular Oncology
- Genetics
Background:
- Ras proteins are key regulators of cell signaling.
- Reactive oxygen species (ROS) are implicated in various cellular processes.
- DNA damage response pathways are crucial for maintaining genomic stability.
Purpose of the Study:
- To investigate the mitogenic properties of Ras-induced ROS.
- To explore the link between ROS, DNA damage response, and cellular proliferation.
- To identify the specific molecular axis responsible for ROS induction.
Main Methods:
- Studies utilizing cultured cells.
- In vivo experiments with zebrafish models.
- Analysis of clinical patient material.
Main Results:
- Ras-induced ROS exhibit mitogenic properties.
- A consistent role for the RAS-RAC1-NOX4 axis was observed across different models.
- This axis is involved in ROS induction, hyperproliferation, and senescence.
Conclusions:
- The RAS-RAC1-NOX4 axis is a critical mediator of Ras-driven cellular changes.
- Understanding this pathway offers insights into cancer development and aging.
- Targeting this axis may have therapeutic implications.
Related Concept Videos
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Radical Autoxidation
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Redox Reactions
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