ArticleCell death & disease2011
Specificity protein, Sp1-mediated increased expression of Prdx6 as a curcumin-induced antioxidant defense in lens epithelial cells against oxidative stress.
Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 66 citations in OpenAlex.
- Loss of Peroxiredoxin 6 Drives Age-Related Klf9/NF-Antioxidants (Basel, Switzerland) · 2026Article
- Comprehensive analysis of RNA sequencing reveals DNA damage response and immune-associated alternative splicing and RBP regulators contributing to preeclampsia.BMC genomics · 2026Article
- Aging, oxidative stress, and cataracts: Therapeutic prospects and translational insights into peroxiredoxin 6.Progress in retinal and eye research · 2026Review
- Plant-Based Care and Therapy in Ophthalmology.Antioxidants (Basel, Switzerland) · 2025Review
- Peroxiredoxin 6 in Stress Orchestration and Disease Interplay.Antioxidants (Basel, Switzerland) · 2025Review
- Therapeutic prospects and potential mechanisms of Prdx6: as a novel target in musculoskeletal disorders.Frontiers in physiology · 2025Review
- Oxidative Stress in Cataract Formation: Is There a Treatment Approach on the Horizon?Antioxidants (Basel, Switzerland) · 2024Review
- Interaction and Collaboration of SP1, HIF-1, and MYC in Regulating the Expression of Cancer-Related Genes to Further Enhance Anticancer Drug Development.Current issues in molecular biology · 2023Review
- Hydralazine Revives Cellular and Ocular Lens Health-Span by Ameliorating the Aging and Oxidative-Dependent Loss of the Nrf2-Activated Cellular Stress Response.Antioxidants (Basel, Switzerland) · 2023Article
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- Peroxiredoxin 6 mediates the protective function of curcumin pretreatment in acute lung injury induced by serum from patients undergoing one-lung ventilation in vitro.BMC pulmonary medicine · 2022Article
- Article
- Engineered Sumoylation-Deficient Prdx6 Mutant Protein-Loaded Nanoparticles Provide Increased Cellular Defense and Prevent Lens Opacity.Antioxidants (Basel, Switzerland) · 2021Article
- Transcriptional reprogramming by oxidative stress occurs within a predefined chromatin accessibility landscape.Free radical biology & medicine · 2021Article
- Peroxiredoxins-The Underrated Actors during Virus-Induced Oxidative Stress.Antioxidants (Basel, Switzerland) · 2021Review
- Dissecting the mechanism of temozolomide resistance and its association with the regulatory roles of intracellular reactive oxygen species in glioblastoma.Journal of biomedical science · 2021Review
- The Protective Effects of Flavonoids in Cataract Formation through the Activation of Nrf2 and the Inhibition of MMP-9.Nutrients · 2020Review
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- Curcumin ameliorates PRMT5-MEP50 arginine methyltransferase expression by decreasing the Sp1 and NF-YA transcription factors in the A549 and MCF-7 cells.Molecular and cellular biochemistry · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Peroxiredoxin 6 (Prdx6) is a pleiotropic oxidative stress-response protein that defends cells against reactive oxygen species (ROS)-induced damage. Curcumin, a naturally occurring agent, has diversified beneficial roles including cytoprotection. Using human lens epithelial cells (hLECs) and Prdx6-deficient cells, we show the evidence that curcumin protects cells by upregulating Prdx6 transcription via invoking specificity protein 1 (Sp1) activity against proapoptotic stimuli. Curcumin enhanced Sp1 and Prdx6 mRNA and protein expression in a concentration-dependent manner, as evidenced by western and real-time PCR analyses, and thereby negatively regulated ROS-mediated apoptosis by blunting ROS expression and lipid peroxidation. Bioinformatic analysis and DNA-protein binding assays disclosed three active Sp1 sites (-19/27, -61/69 and -82/89) in Prdx6 promoter. Co-transfection experiments with Sp1 and Prdx6 promoter-chloramphenicol acetyltransferase (CAT) constructs showed that CAT activity was dramatically increased in LECs or Sp1-deficient cells (SL2). Curcumin treatment of LECs enhanced Sp1 binding to its sites, consistent with curcumin-dependent stimulation of Prdx6 promoter with Sp1 sites and cytoprotection. Notably, disruption of Sp1 sites by point mutagenesis abolished curcumin transactivation of Prdx6. Also, curcumin failed to activate Prdx6 expression in the presence of Sp1 inhibitors, demonstrating that curcumin-mediated increased expression of Prdx6 was dependent on Sp1 activity. Collectively, the study may provide a foundation for developing transcription-based inductive therapy to reinforce endogenous antioxidant defense by using dietary supplements.
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