The DOI matches its Crossref record; 64 of the 64 references it cites were found in a registry or an index.
Expanding roles of superoxide dismutases in cell regulation and cancer
Open accessAbstract
Reactive oxygen species (ROS) have important roles in normal physiology and diseases, particularly cancer. Under normal physiological conditions, they participate in redox reactions and serve as second messengers for regulatory functions. Owing to aberrant metabolism, cancer cells accumulate excessive ROS, thus requiring a robustly active antioxidant system to prevent cellular damage. Superoxide dismutases (SODs) are enzymes that catalyze the removal of superoxide free radicals. There are three distinct members of this metalloenzyme family in mammals: SOD1 (Cu/ZnSOD), SOD2 (MnSOD) and SOD3 (ecSOD). SODs are increasingly recognized for their regulatory functions in growth, metabolism and oxidative stress responses, which are also crucial for cancer development and survival. Growing evidence shows that SODs are also potentially useful anticancer drug targets. This review will focus on recent research of SODs in cellular regulation, with emphasis on their roles in cancer biology and therapy.
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Otto Warburg's contributions to current concepts of cancer metabolism
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Cited by
Siska, P. J., Beckermann, K. E., Mason, F. M., Andrejeva, G., Greenplate, A. R., Sendor, A. B., Chiang, Y.-C. J., Corona, A. L., Gemta, L. F., Vincent, B. G., et al. (2017) · JCI Insight · doi:10.1172/jci.insight.93411 · Cited by 389
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Mendes, C., & Serpa, J. (2019) · Antioxidants · doi:10.3390/antiox8120603 · Cited by 21
Metadata
- Authors
- Che, M., Wang, R., Li, X., Wang, H.-Y., & Zheng, X. F. S.
- Venue
- Drug Discovery Today
- Publisher
- Elsevier BV
- Published
- 2016-01
- Volume
- 21
- Issue
- 1
- Pages
- 143-149
- ISSN
- 1359-6446 (ISSN-L)
- OpenAlex
- W1759734542
- Cited by
- 270
- References
- 64
- FWCI
- 6.18
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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