ArticleOncogene2023
Chronic hypoxia favours adoption to a castration-resistant cell state in prostate cancer.
Article in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The trial behind it
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- The clinical landscape of HIF2α inhibitors in oncology.Nature reviews. Clinical oncology · 2026Review
- Review
- Pathology of a Canine Model of Localized Prostate Carcinoma.The Prostate · 2026Article
- A bioinformatics screen identifies TCF19 as an aggressiveness-sustaining gene in prostate cancer.Molecular oncology · 2025Article
- Hypoxia-Driven Extracellular Vesicles Promote Pro-Metastatic Signalling in LNCaP Cells via Wnt and EMT Pathways.Biology · 2025Article
- Article
- Article
- Tumour hypoxia in driving genomic instability and tumour evolution.Nature reviews. Cancer · 2025Review
- The zinc finger protein560(ZNF560) functions as a novel oncogenic gene in osteosarcoma.Scientific reports · 2025Article
- Acute Three-Dimensional Hypoxia Regulates Angiogenesis.Advanced healthcare materials · 2025Article
- Hypoxic Regulation of the KLK4 Gene in two Different Prostate Cancer Cells Treated with TGF- β.Cell biochemistry and biophysics · 2024Article
- Long-term severe hypoxia adaptation induces non-canonical EMT and a novel Wilms Tumor 1 (WT1) isoform.Cancer gene therapy · 2024Article
- A Compound That Inhibits Glycolysis in Prostate Cancer Controls Growth of Advanced Prostate Cancer.Molecular cancer therapeutics · 2024Article
- Obesity, dietary interventions and microbiome alterations in the development and progression of prostate cancer.Frontiers in immunology · 2024Review
- Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Predicting and treating recurrence in intermediate-risk prostate cancer patients remains a challenge despite having identified genomic instability [1] and hypoxia [2, 3] as risk factors. This underlies challenges in assigning the functional impact of these risk factors to mechanisms promoting prostate cancer progression. Here we show chronic hypoxia (CH), as observed in prostate tumours [4], leads to the adoption of an androgen-independent state in prostate cancer cells. Specifically, CH results in prostate cancer cells adopting transcriptional and metabolic alterations typical of castration-resistant prostate cancer cells. These changes include the increased expression of transmembrane transporters for the methionine cycle and related pathways leading to increased abundance of metabolites and expression of enzymes related to glycolysis. Targeting of the Glucose Transporter 1 (GLUT1) identified a dependency on glycolysis in androgen-independent cells. Overall, we identified a therapeutically targetable weakness in chronic hypoxia and androgen-independent prostate cancer. These findings may offer additional strategies for treatment development against hypoxic prostate cancer.
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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.