Peroxiredoxin 1 – an antioxidant enzyme in cancer
Open accessAbstract
Peroxiredoxins (PRDX s), a ubiquitous family of redox‐regulating proteins, are reported of potential to eliminate various reactive oxygen species (ROS). As a major member of the antioxidant enzymes, PRDX 1 can become easily over‐oxidized on its catalytically active cysteine induced by a variety of stimuli in vitro and in vivo. In nucleus, oligomeric PRDX 1 directly associates with p53 or transcription factors such as c‐Myc, NF‐κB and AR, and thus affects their bioactivities upon gene regulation, which in turn induces or suppresses cell death. Additionally, PRDX 1 in cytoplasm has anti‐apoptotic potential through direct or indirect interactions with several ROS‐dependent (redox regulation) effectors, including ASK 1, p66 Shc, GST pi/JNK and c‐Abl kinase. PRDX 1 is proven to be a versatile molecule regulating cell growth, differentiation and apoptosis. Recent studies have found that PRDX 1 and/or PRDX 1‐regulated ROS‐dependent signalling pathways play an important role in the progression and metastasis of human tumours, particularly in breast, oesophageal and lung cancers. In this paper, we review the structure, effector functions of PRDX 1, its role in cancer and the pivotal role of ROS in anticancer treatment.
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PRDX1 is a hub of the MSN module and a family member of antioxidant enzymes implicated in protective cellular responses.
“Peroxiredoxin 1 (PRDX1), another hub of this module, is a family member of antioxidant enzymes also implicated in protective cellular responses [125].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [125]
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Research works printed but not linked: 1
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Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau
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- Authors
- Ding, C., Fan, X., & Wu, G.
- Affiliations
- Southeast University (CN)
- Zhongda Hospital Southeast University (CN)
- Corresponding author
- Wu, Guoqiu
- Venue
- Journal of Cellular and Molecular Medicine
- Publisher
- Wiley
- Published
- 2016-09-21
- Volume
- 21
- Issue
- 1
- Pages
- 193-202
- ISSN
- 1582-1838 (ISSN-L)
- 1582-4934
- PMC
- PMC5192802
- OpenAlex
- W2521925016
- Cited by
- 232
- References
- 131
- Citations by year
- 2026: 21 · 2025: 35 · 2024: 23 · 2023: 28 · 2022: 26 · 2021: 30 · 2020: 22 · 2019: 22 · 2018: 15 · 2017: 9 · 2016: 1
- FWCI
- 1.42
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Cellular and Molecular Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (30970809, 81271636)
- Natural Science Foundation of Jiangsu Province (BK2009274)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Keywords
- peroxiredoxin 1, antioxidant enzymes, reactive oxygen species, redox regulation, cancer, apoptosis, p53, c-Myc, NF-κB, androgen receptor, ASK1, p66Shc, JNK, c-Abl kinase, glutathione S-transferase pi, tumor progression, metastasis, breast cancer, esophageal cancer, lung cancer, anticancer treatment
- MeSH terms
- Antioxidants, Humans, Neoplasms, Oxidation-Reduction, Signal Transduction, Reactive Oxygen Species, Peroxiredoxins
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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