ArticleBritish journal of cancer2016
Androgen deprivation in LNCaP prostate tumour xenografts induces vascular changes and hypoxic stress, resulting in promotion of epithelial-to-mesenchymal transition.
Article in British journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Randomized Phase 2 Trial of Presurgical Androgen Deprivation Therapy With or Without Axitinib in Prostate Cancer Presenting With Lymph Node Metastasis.European urology oncology · 2025Trial
- Targeting secreted PLACell death & disease · 2025Article
- Review
- Molecular Hallmarks of Prostate-specific Membrane Antigen in Treatment-naïve Prostate Cancer.European urology · 2024Article
- CDK9 inhibition inhibits multiple oncogenic transcriptional and epigenetic pathways in prostate cancer.British journal of cancer · 2024Article
- Prohibitin Links Cell Cycle, Motility and Invasion in Prostate Cancer Cells.International journal of molecular sciences · 2023Article
- MiR-21 Is Induced by Hypoxia and Down-RegulatesCancers · 2023Article
- Understanding human aging and the fundamental cell signaling link in age-related diseases: the middle-aging hypovascularity hypoxia hypothesis.Frontiers in aging · 2023Article
- Targeting DNA topoisomerase IIα (TOP2A) in the hypoxic tumour microenvironment using unidirectional hypoxia-activated prodrugs (uHAPs).IUBMB life · 2023Review
- Attenuating Adaptive VEGF-A and IL8 Signaling Restores Durable Tumor Control in AR Antagonist-Treated Prostate Cancers.Molecular cancer research : MCR · 2022Article
- Hypoxic Signaling Is Modulated by Calcium Channel, CaV1.3, in Androgen-Resistant Prostate Cancer.Bioelectricity · 2022Article
- Dissecting the effects of androgen deprivation therapy on cadherin switching in advanced prostate cancer: A molecular perspective.Oncology research · 2022Review
- Circulating Tumour Cells Indicate the Presence of Residual Disease Post-Castration in Prostate Cancer Patient-Derived Xenograft Models.Frontiers in cell and developmental biology · 2022Article
- Emerging Role of Extracellular Vesicles in Prostate Cancer.Endocrinology · 2021Review
- The clinical guiding value of a radiomics model for androgen deprivation therapy for prostate cancer.The Journal of international medical research · 2021Article
- Cellular rewiring in lethal prostate cancer: the architect of drug resistance.Nature reviews. Urology · 2020Review
- Androgen-regulated transcription ofeLife · 2019Article
- H19-Dependent Transcriptional Regulation of β3 and β4 Integrins Upon Estrogen and Hypoxia Favors Metastatic Potential in Prostate Cancer.International journal of molecular sciences · 2019Article
- Tumor Cell Dormancy and Reactivation in Bone: Skeletal Biology and Therapeutic Opportunities.JBMR plus · 2019Review
- Engineering osteoblastic metastases to delineate the adaptive response of androgen-deprived prostate cancer in the bone metastatic microenvironment.Bone research · 2019Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWhen single-agent androgen deprivation therapy (ADT) is administered for locally advanced prostate cancer, men usually relapse within 1-2 years with more malignant castrate-resistant disease. The reason for this is currently unknown. We now hypothesise that an initial treatment response that increases tumour hypoxia drives selection of more malignant tumours.
methodsThe LNCaP prostate tumour xenografts were analysed for physiological (oxygen and vasculature) and genetic (PCR array) changes during longitudinal treatment with ADT (bicalutamide, 6 or 2 mg kg⁻¹ daily for 28 days).
resultsBicalutamide caused an immediate (within 24 h) dose-dependent fall in oxygenation in LNCaP-luc prostate tumours with a nadir of ≤ 0.1% oxygen within 3-7 days; this was attributed to a significant loss of tumour microvessels (window chamber study). The hypoxic nadir persisted for 10-14 days. During the next 7 days, tumours regrew, oxygenation improved and the vasculature recovered; this was inhibited by the VEGF inhibitor B20.4.1.1. Gene expression over 28 days showed marked fluctuations consistent with the physiological changes. Accompanying the angiogenic burst (day 21) was a particularly striking increase in expression of genes associated with epithelial-to-mesenchymal transition (EMT). In particular, insulin-like growth factor 1 (IGF-1) showed increases in mRNA and protein expression.
conclusionsHypoxic stress caused by ADT promotes EMT, providing a mechanism for the cause of malignant progression in prostate cancer.
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