ArticleThe Journal of biological chemistry2014
Hydrogen sulfide represses androgen receptor transactivation by targeting at the second zinc finger module.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 84 citations in OpenAlex.
- The first and second zinc finger domains from Poly-ADP-ribose polymerase 1 (PARP1) are modified by hydrogen sulfide.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Article
- Persulfidation of the zinc finger protein ZRANB2 modulates its RNA binding and alternative splicing function.Journal of inorganic biochemistry · 2026Article
- A Dinuclear Iron(II) Persulfide Complex Reacts with OJournal of the American Chemical Society · 2026Article
- HBiochemistry · 2026Article
- Article
- Hydrogen sulfide (H2S) coordinates redox balance, carbon metabolism, and mitochondrial bioenergetics to suppress SARS-CoV-2 infection.PLoS pathogens · 2025Article
- Bio-Pathological Functions of Posttranslational Modifications of Histological Biomarkers in Breast Cancer.Molecules (Basel, Switzerland) · 2024Review
- Chemoselective Proteomics, Zinc Fingers, and a Zinc(II) Model for HAngewandte Chemie (International ed. in English) · 2024Article
- Mining proteomes for zinc finger persulfidation.RSC chemical biology · 2024Article
- Therapeutic Potential of Hydrogen Sulfide in Reproductive System Disorders.Biomolecules · 2024Review
- Role of hydrogen sulfide in the male reproductive system.Frontiers in endocrinology · 2024Review
- Cysteine-rich zinc finger proteins and the nuclear factor kappa-B pathway.Frontiers in chemical biology · 2024Article
- Hydrogen sulfide and its potential as a possible therapeutic agent in male reproduction.Frontiers in endocrinology · 2024Review
- Recent advances in the role of endogenous hydrogen sulphide in cancer cells.Cell proliferation · 2023Review
- Hydrogen sulfide and metal interaction: the pathophysiological implications.Molecular and cellular biochemistry · 2022Review
- Reactive Sulfur Compounds in the Fight against COVID-19.Antioxidants (Basel, Switzerland) · 2022Review
- Targeting Zinc Finger Proteins with Exogenous Metals and Molecules: Lessons learned from Tristetraprolin, a CCCH type Zinc Finger.European journal of inorganic chemistry · 2021Article
- Molecular Functions of Hydrogen Sulfide in Cancer.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Review
- Hydrogen Sulfide Inhibits TMPRSS2 in Human Airway Epithelial Cells: Implications for SARS-CoV-2 Infection.Biomedicines · 2021Article
- Hydrogen Sulfide-Clues from Evolution and Implication for Neonatal Respiratory Diseases.Children (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Androgen receptor (AR) signaling is indispensable for the development of prostate cancer from the initial androgen-dependent state to a later aggressive androgen-resistant state. This study examined the role of hydrogen sulfide (H(2)S), a novel gasotransmitter, in the regulation of AR signaling as well as its mediation in androgen-independent cell growth in prostate cancer cells. Here we found that H(2)S inhibits cell proliferation of both androgen-dependent (LNCaP) and antiandrogen-resistant prostate cancer cells (LNCaP-B), with more significance on the latter, which was established by long term treatment of parental LNCaP cells with bicalutamide. The expression of cystathionine γ-lyase (CSE), a major H(2)S producing enzyme in prostate tissue, was reduced in both human prostate cancer tissues and LNCaP-B cells. LNCaP-B cells were resistant to bicalutamide-induced cell growth inhibition, and CSE overexpression could rebuild the sensitivity of LNCaP-B cells to bicalutamide. H(2)S significantly repressed the expression of prostate-specific antigen (PSA) and TMPRSS2, two AR-targeted genes. In addition, H(2)S inhibited AR binding with PSA promoter and androgen-responsive element (ARE) luciferase activity. We further found that AR is post-translationally modified by H(2)S through S-sulfhydration. Mutation of cysteine 611 and cysteine 614 in the second zinc finger module of AR-DNA binding domain diminished the effects of H(2)S on AR S-sulfhydration and AR dimerization. These data suggest that reduced CSE/H2S signaling contributes to antiandrogen-resistant status, and sufficient level of H(2)S is able to inhibit AR transactivation and treat castration-resistant prostate cancer.
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Registered trials
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