ArticleCancer research2009
Inhibition of activator protein-1 by sulforaphane involves interaction with cysteine in the cFos DNA-binding domain: implications for chemoprevention of UVB-induced skin cancer.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 77 citations in OpenAlex.
- Nanocarrier-Enabled Delivery of Glucosinolates for Skin Cancer Prevention and Therapy.The AAPS journal · 2026Review
- Sulforaphane as a Photoprotective Agent Against UV-Induced Skin Damage and Carcinogenesis: A Scoping Review.Journal of personalized medicine · 2026Review
- Potential dietary geroprotectors and their impact on key mechanisms of aging.Biogerontology · 2025Review
- The Multifaceted Health Benefits of Broccoli-A Review of Glucosinolates, Phenolics and Antimicrobial Peptides.Molecules (Basel, Switzerland) · 2025Review
- Review
- A recent update on the connection between dietary phytochemicals and skin cancer: emerging understanding of the molecular mechanism.Annals of medicine and surgery (2012) · 2024Review
- Anti-Inflammatory Therapeutic Mechanisms of Isothiocyanates: Insights from Sulforaphane.Biomedicines · 2024Review
- Inhibition of UV-Induced Stress Signaling and Inflammatory Responses in SKH-1 Mouse Skin by Topical Small-Molecule PD-L1 Blockade.JID innovations : skin science from molecules to population health · 2024Article
- Article
- The Drinking Water and Swimming Pool Disinfectant Trichloroisocyanuric Acid Causes Chlorination Stress Enhancing Solar UV-Induced Inflammatory Gene Expression in AP-1 Transgenic SKH-1 Luciferase Reporter Mouse Skin.Photochemistry and photobiology · 2023Article
- Current perspectives of mitochondria-targeted antioxidants in cancer prevention and treatment.Frontiers in cell and developmental biology · 2023Review
- Mechanistic review of sulforaphane as a chemoprotective agent in bladder cancer.American journal of clinical and experimental urology · 2023Review
- Identification of the NRF2 transcriptional network as a therapeutic target for trigeminal neuropathic pain.Science advances · 2022Article
- NRF2 in dermatological disorders: Pharmacological activation for protection against cutaneous photodamage and photodermatosis.Free radical biology & medicine · 2022Review
- Topical hypochlorous acid (HOCl) blocks inflammatory gene expression and tumorigenic progression in UV-exposed SKH-1 high risk mouse skin.Redox biology · 2021Article
- Prevention of Skin Carcinogenesis by the Non-β-blocking R-carvedilol Enantiomer.Cancer prevention research (Philadelphia, Pa.) · 2021Article
- Covalent Modification of Proteins by Plant-Derived Natural Products: Proteomic Approaches and Biological Impacts.Proteomics · 2021Review
- Pathogenic and therapeutic role for NRF2 signaling in ultraviolet light-induced skin pigmentation.JCI insight · 2020Article
- Epigenome, Transcriptome, and Protection by Sulforaphane at Different Stages of UVB-Induced Skin Carcinogenesis.Cancer prevention research (Philadelphia, Pa.) · 2020Article
- Nrf2 in cancers: A double-edged sword.Cancer medicine · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Sulforaphane is an isothiocyanate derived from cruciferous vegetables that has been linked to decreased risk of certain cancers. Although the role of sulforaphane in the induction of the transcription factor Nrf2 has been studied extensively, there is also evidence that inhibition of the transcription factor activator protein-1 (AP-1) may contribute to the chemopreventive properties of this compound. In this study, we show for the first time that sulforaphane is effective at reducing the multiplicity and tumor burden of UVB-induced squamous cell carcinoma in a mouse model using cotreatment with the compound and the carcinogen. We also show that sulforaphane pretreatment is able to reduce the activity of AP-1 luciferase in the skin of transgenic mice after UVB. Chromatin immunoprecipitation analysis verified that a main constituent of the AP-1 dimer, cFos, is inhibited from binding to the AP-1 DNA binding site by sulforaphane. Electrophoretic mobility shift assay analysis of nuclear proteins also shows that sulforaphane and diamide, both known to react with cysteine amino acids, are effective at inhibiting AP-1 from binding to its response element. Using truncated recombinant cFos and cJun, we show that mutation of critical cysteines in the DNA-binding domain of these proteins (Cys(154) in cFos and Cys(272) in cJun) results in loss of sensitivity to both sulforaphane and diamide in electrophoretic mobility shift assay analysis. Together, these data indicate that inhibition of AP-1 activity may be an important molecular mechanism in chemoprevention of squamous cell carcinoma by sulforaphane.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.