ArticleInternational journal of molecular sciences2019
Heme Oxygenase 1 Impairs Glucocorticoid Receptor Activity in Prostate Cancer.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- The Regulation of Catecholamine Biosynthesis by the Gas Transmitters Carbon Monoxide and Hydrogen Sulfide.Current issues in molecular biology · 2025Article
- Blood matters: the hematological signatures of Coronavirus infection.Cell death & disease · 2024Article
- The Growth Inhibitory Effect of Resveratrol and Gallic Acid on Prostate Cancer Cell Lines through the Alteration of Oxidative Stress Balance: The Interplay betweenAnti-cancer agents in medicinal chemistry · 2024Article
- Pharmacological Significance of Heme Oxygenase 1 in Prostate Cancer.Current issues in molecular biology · 2023Review
- Non-canonical vs. Canonical Functions of Heme Oxygenase-1 in Cancer.Journal of cancer prevention · 2022Review
- Role ofInternational journal of molecular sciences · 2021Article
- Scavenging of Labile Heme by Hemopexin Is a Key Checkpoint in Cancer Growth and Metastases.Cell reports · 2020Article
- HO-1 Interactors Involved in the Colonization of the Bone Niche: Role of ANXA2 in Prostate Cancer Progression.Biomolecules · 2020Article
- α-Actinin-4 Promotes the Progression of Prostate Cancer Through the Akt/GSK-3β/β-Catenin Signaling Pathway.Frontiers in cell and developmental biology · 2020Article
- Editorial of Special Issue "Protective and Detrimental Role of Heme Oxygenase-1".International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Glucocorticoids are used during prostate cancer (PCa) treatment. However, they may also have the potential to drive castration resistant prostate cancer (CRPC) growth via the glucocorticoid receptor (GR). Given the association between inflammation and PCa, and the anti-inflammatory role of heme oxygenase 1 (HO-1), we aimed at identifying the molecular processes governed by the interaction between HO-1 and GR. PCa-derived cell lines were treated with Hemin, Dexamethasone (Dex), or both. We studied GR gene expression by RTqPCR, protein expression by Western Blot, transcriptional activity using reporter assays, and nuclear translocation by confocal microscopy. We also evaluated the expression of HO-1, FKBP51, and FKBP52 by Western Blot. Hemin pre-treatment reduced Dex-induced GR activity in PC3 cells. Protein levels of FKBP51, a cytoplasmic GR-binding immunophilin, were significantly increased in Hemin+Dex treated cells, possibly accounting for lower GR activity. We also evaluated these treatments in vivo using PC3 tumors growing as xenografts. We found non-significant differences in tumor growth among treatments. Immunohistochemistry analyses revealed strong nuclear GR staining in almost all groups. We did not observe HO-1 staining in tumor cells, but high HO-1 reactivity was detected in tumor infiltrating macrophages. Our results suggest an association and crossed modulation between HO-1 and GR pathways.
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