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Updated: Feb 24, 2026
Production and Detection of Reactive Oxygen Species ROS in Cancers
Published on: November 21, 2011
Extracellular superoxide dismutase and its role in cancer
Brandon Griess1, Eric Tom1, Frederick Domann2
1Department of Biochemistry and Molecular Biology, Buffett Cancer Center, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198, United States.
Abstract:
Reactive oxygen species (ROS) are increasingly recognized as critical determinants of cellular signaling and a strict balance of ROS levels must be maintained to ensure proper cellular function and survival. Notably, ROS is increased in cancer cells. The superoxide dismutase family plays an essential physiological role in mitigating deleterious effects of ROS. Due to the compartmentalization of ROS signaling, EcSOD, the only superoxide dismutase in the extracellular space, has unique characteristics and functions in cellular signal transduction. In comparison to the other two intracellular SODs, EcSOD is a relatively new comer in terms of its tumor suppressive role in cancer and the mechanisms involved are less well understood. Nevertheless, the degree of differential expression of this extracellular antioxidant in cancer versus normal cells/tissues is more pronounced and prevalent than the other SODs. A significant association of low EcSOD expression with reduced cancer patient survival further suggests that loss of extracellular redox regulation promotes a conducive microenvironment that favors cancer progression. The vast array of mechanisms reported in mediating deregulation of EcSOD expression, function, and cellular distribution also supports that loss of this extracellular antioxidant provides a selective advantage to cancer cells. Moreover, overexpression of EcSOD inhibits tumor growth and metastasis, indicating a role as a tumor suppressor. This review focuses on the current understanding of the mechanisms of deregulation and tumor suppressive function of EcSOD in cancer.
Insights
Extracellular superoxide dismutase (EcSOD) acts as a tumor suppressor by regulating reactive oxygen species (ROS) in cancer. Loss of EcSOD promotes cancer progression, while its overexpression inhibits tumor growth.
Area of Science:
- Biochemistry
- Oncology
- Cellular Biology
Background:
- Reactive oxygen species (ROS) are crucial for cellular signaling, requiring balanced levels for proper function.
- Elevated ROS levels are characteristic of cancer cells.
- The superoxide dismutase (SOD) family mitigates ROS damage, with extracellular SOD (EcSOD) playing a unique role due to its location.
Purpose of the Study:
- To review the mechanisms of deregulation and tumor-suppressive functions of EcSOD in cancer.
- To highlight EcSOD's distinct role compared to intracellular SODs.
- To underscore the significance of extracellular redox regulation in cancer progression.
Main Methods:
- Literature review focusing on EcSOD's expression, function, and distribution in cancer.
- Analysis of studies investigating the association between EcSOD levels and cancer patient survival.
- Examination of mechanisms underlying EcSOD deregulation in neoplastic cells.
Main Results:
- EcSOD exhibits more pronounced differential expression in cancer than other SODs.
- Low EcSOD expression correlates with reduced patient survival, indicating a pro-tumorigenic microenvironment.
- Deregulation of EcSOD provides a selective advantage to cancer cells, promoting growth and metastasis.
- EcSOD overexpression demonstrates tumor-suppressive activity, inhibiting tumor growth and metastasis.
Conclusions:
- EcSOD is a critical extracellular antioxidant with significant tumor-suppressive functions in cancer.
- Loss of EcSOD contributes to a pro-cancerous microenvironment through impaired redox regulation.
- Understanding EcSOD deregulation mechanisms is key to developing novel cancer therapies targeting extracellular redox balance.
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