Imperative connotation of SODs in cancer: Emerging targets and multifactorial role of action
Superoxide dismutase (SOD) is a crucial enzyme responsible for the redox homeostasis inside the cell. As a part of the antioxidant defense system, it plays a pivotal role in the dismutation of the superoxide radicals (O2−) generated mainly by the oxidative phosphorylation, which would otherwise brin...
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Published in: | IUBMB life Vol. 76; no. 9; pp. 592 - 613 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Hoboken, USA
John Wiley & Sons, Inc
01-09-2024
Wiley Subscription Services, Inc |
Subjects: | |
Online Access: | Get full text |
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Summary: | Superoxide dismutase (SOD) is a crucial enzyme responsible for the redox homeostasis inside the cell. As a part of the antioxidant defense system, it plays a pivotal role in the dismutation of the superoxide radicals (O2−) generated mainly by the oxidative phosphorylation, which would otherwise bring out the redox dysregulation, leading to higher reactive oxygen species (ROS) generation and, ultimately, cell transformation, and malignancy. Several studies have shown the involvement of ROS in a wide range of human cancers. As SOD is the key enzyme in regulating ROS, any change, such as a transcriptional change, epigenetic remodeling, functional alteration, and so forth, either activates the proto‐oncogenes or aberrant signaling cascades, which results in cancer. Interestingly, in some cases, SODs act as tumor promoters instead of suppressors. Furthermore, SODs have also been known to switch their role during tumor progression. In this review, we have tried to give a comprehensive account of SODs multifactorial role in various human cancers so that SODs‐based therapeutic strategies could be made to thwart cancers. |
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Bibliography: | Biswajit Panda, Ankita Tripathy and Srimanta Patra contributed equally to this work. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
ISSN: | 1521-6543 1521-6551 1521-6551 |
DOI: | 10.1002/iub.2821 |