ReviewCancer drug resistance (Alhambra, Calif.)2021
Oxidative stress and redox signaling in CRPC progression: therapeutic potential of clinically-tested Nrf2-activators.
Review in Cancer drug resistance (Alhambra, Calif.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Targeting ALDH7A1 with covalent inhibitors reveals new chemical space for prostate cancer therapy.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Antioxidant Properties of Novel Lipophilic Fluoroquinolone Compounds Against Oxidative Stress Induced by Acetaminophen and Carbon Tetrachloride in Male Wistar Rats.Biomolecules · 2026Article
- Mechanism and therapeutic significance of ARV-110 combined with a PDGFR inhibitor for the induction of apoptosis in castration-resistant prostate cancer cells through the ROS/JNK pathway.Cell death & disease · 2026Article
- Quercetin Inhibits AKT Ser473 Phosphorylation and Disrupts AKT-Androgen Receptor Signaling in Castration-Resistant Prostate Cancer Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Intermittent Fasting and Androgen Receptor Signaling in Prostate Cancer: Metabolic Crosstalk and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Mitochondrial convergence of ferroptosis and cuproptosis in castration-resistant prostate cancer: From metabolic vulnerabilities to therapeutic targeting.BBA advances · 2026Review
- Oxidative stress reactivates androgen receptor signaling via USP36 to drive castration resistance in prostate cancer.Scientific reports · 2025Article
- Interplay between Nrf2 and ROS in regulating epithelial-mesenchymal transition: implications for cancer metastasis and therapy.Molecular biology reports · 2025Review
- Prostate cancer exploits BRD9-driven metabolic reprogramming to shape the aggressive phenotype.Cell death & disease · 2025Article
- Lanatoside C Inhibits Proliferation and Induces Apoptosis in Human Prostate Cancer Cells Through the TNF/IL-17 Signaling Pathway.International journal of molecular sciences · 2025Article
- Mendelian Randomization Identifies CD25+ CD4+ Tregs and Plasma Proteins in Androgenetic Alopecia Pathogenesis.Clinical, cosmetic and investigational dermatology · 2025Article
- Heme Oxygenase-1 and Prostate Cancer: Function, Regulation, and Implication in Cancer Therapy.International journal of molecular sciences · 2024Review
- Alpha-Lipoic Acid Reduces Cell Growth, Inhibits Autophagy, and Counteracts Prostate Cancer Cell Migration and Invasion: Evidence from In Vitro Studies.International journal of molecular sciences · 2023Article
- Role of Natural and Synthetic Compounds in Modulating NRF2/KEAP1 Signaling Pathway in Prostate Cancer.Cancers · 2023Review
- Pharmacological Significance of Heme Oxygenase 1 in Prostate Cancer.Current issues in molecular biology · 2023Review
- Metabolic changes during prostate cancer development and progression.Journal of cancer research and clinical oncology · 2023Review
- The ERα-NRF2 signalling axis promotes bicalutamide resistance in prostate cancer.Cell communication and signaling : CCS · 2022Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Androgen deprivation therapy (ADT) is the mainstay regimen in patients with androgen-dependent prostate cancer (PCa). However, the selection of androgen-independent cancer cells leads to castrate resistant prostate cancer (CRPC). The aggressive phenotype of CRPC cells underscores the need to elucidate mechanisms and therapeutic strategies to suppress CRPC outgrowth. Despite ADT, the activation of androgen receptor (AR) transcription factor continues via crosstalk with parallel signaling pathways. Understanding of how these signaling cascades are initiated and amplified post-ADT is lacking. Hormone deprivation can increase oxidative stress and the resultant reactive oxygen species (ROS) may activate both AR and non-AR signaling. Moreover, ROS-induced inflammatory cytokines may further amplify these redox signaling pathways to augment AR function. However, clinical trials using ROS quenching small molecule antioxidants have not suppressed CRPC progression, suggesting that more potent and persistent suppression of redox signaling in CRPC cells will be needed. The transcription factor Nrf2 increases the expression of numerous antioxidant enzymes and downregulates the function of inflammatory transcription factors, e.g., nuclear factor kappa B. We documented that Nrf2 overexpression can suppress AR-mediated transcription in CRPC cell lines. Furthermore, two Nrf2 activating agents, sulforaphane (a phytochemical) and bardoxolone-methyl (a drug in clinical trial) suppress AR levels and sensitize CRPC cells to anti-androgens. These observations implicate the benefits of potent Nrf2-activators to suppress the lethal signaling cascades that lead to CRPC outgrowth. This review article will address the redox signaling networks that augment AR signaling during PCa progression to CRPC, and the possible utility of Nrf2-activating agents as an adjunct to ADT.
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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.