دورية أكاديمية
Chronic hypoxia favours adoption to a castration-resistant cell state in prostate cancer.
العنوان: | Chronic hypoxia favours adoption to a castration-resistant cell state in prostate cancer. |
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المؤلفون: | Cameron S; Princess Margaret Cancer Research Centre, Toronto, ON, Canada., Deblois G; Princess Margaret Cancer Research Centre, Toronto, ON, Canada.; Institute for Research in Immunology and Cancer (IRIC), Faculty of Pharmacy, University of Montréal, Montréal, QC, H3T 1J4, Canada., Hawley JR; Princess Margaret Cancer Research Centre, Toronto, ON, Canada.; Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada., Qamra A; Princess Margaret Cancer Research Centre, Toronto, ON, Canada., Zhou S; Princess Margaret Cancer Research Centre, Toronto, ON, Canada.; Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada., Tonekaboni SAM; Princess Margaret Cancer Research Centre, Toronto, ON, Canada.; Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada., Murison A; Princess Margaret Cancer Research Centre, Toronto, ON, Canada., Van Vliet R; Princess Margaret Cancer Research Centre, Toronto, ON, Canada., Liu J; Duke University School of Medicine, Durham, NC, USA., Locasale JW; Duke University School of Medicine, Durham, NC, USA., Lupien M; Princess Margaret Cancer Research Centre, Toronto, ON, Canada. Mathieu.Lupien@uhnresearch.ca.; Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada. Mathieu.Lupien@uhnresearch.ca.; Ontario Institute for Cancer Research, Toronto, ON, Canada. Mathieu.Lupien@uhnresearch.ca. |
المصدر: | Oncogene [Oncogene] 2023 May; Vol. 42 (21), pp. 1693-1703. Date of Electronic Publication: 2023 Apr 05. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: Nature Publishing Group Country of Publication: England NLM ID: 8711562 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5594 (Electronic) Linking ISSN: 09509232 NLM ISO Abbreviation: Oncogene Subsets: MEDLINE |
أسماء مطبوعة: | Publication: <2002->: Basingstoke : Nature Publishing Group Original Publication: Basingstoke, Hampshire, UK : Scientific & Medical Division, MacMillan Press, c1987- |
مواضيع طبية MeSH: | Prostatic Neoplasms, Castration-Resistant*/pathology , Prostatic Neoplasms*/pathology, Male ; Humans ; Androgens/metabolism ; Prostate/pathology ; Hypoxia/metabolism ; Castration ; Receptors, Androgen/genetics ; Cell Line, Tumor |
مستخلص: | 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. (© 2023. The Author(s).) |
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معلومات مُعتمدة: | FRN-153234 Gouvernement du Canada | Instituts de Recherche en Santé du Canada | CIHR Skin Research Training Centre (Skin Research Training Centre) |
المشرفين على المادة: | 0 (Androgens) 0 (Receptors, Androgen) |
تواريخ الأحداث: | Date Created: 20230405 Date Completed: 20230524 Latest Revision: 20230525 |
رمز التحديث: | 20230525 |
مُعرف محوري في PubMed: | PMC10202808 |
DOI: | 10.1038/s41388-023-02680-z |
PMID: | 37020039 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1476-5594 |
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DOI: | 10.1038/s41388-023-02680-z |