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The Yin Yang Role of Nitric Oxide in Prostate Cancer

Datos Bibliográficos

ID21748479
AutoresYash Soni (0000-0001-9944-9972, University of Miami), Kenneth Softness (0000-0002-4592-8406, Beth Israel Deaconess Medical Center), Himanshu Arora (0000-0002-8013-6033, University of Miami, autor de correspondencia), Ranjith Ramasamy (0000-0003-1387-7904, University of Miami, autor de correspondencia)
Año2020
Volumen14
Número1
Páginas1557988320903191-1557988320903191
Fecha de publicación2020-01-01
Open AccessSí
TipoARTICLE
RevistaAmerican Journal of Men s Health (JOURNAL)
Identificadores de la revistaISSN: 1557-9883 • E-ISSN: 1557-9891
EditorialSAGE Publications (PUBLISHER • US)
DOI10.1177/1557988320903191
PMID32028831
OpenAlexW3005402334
IdiomaEN
Referencias citadas36

Nitric oxide (NO) is a ubiquitous signaling molecule in the human body with well-known roles in many different processes and organ systems. In cancer, the two-concentrations hypothesis of NO has dictated that low levels of NO are cancer promoting, while high levels of NO are protective against cancer. Although prostate cancer is a hormonally driven malignancy, research has been shifting away from androgen-responsive epithelial cells and evolving to focus on NO therapies, the tumor microenvironment (TME), and inflammation. NO is reported to be able to inhibit activity of the androgen receptor. This may prevent prostate growth, but low levels of NO could conversely select for castration-resistant prostate cells, creating an aggressive cancer phenotype. At high levels, nitrosative stress created from NO overproduction can be protective against prostate neoplasia. In this review, we discuss development and possibilities of NO-based therapies for prostate cancer

Androgen · Androgen receptor · Cancer · Hormone · Inflammation · Malignancy · Nitric oxide · Prostate · Prostate cancer · Tumor microenvironment · Cancer, Hypoxia, and Metabolism · Eicosanoids and Hypertension Pharmacology · Medicine · Nitric Oxide and Endothelin Effects · Cancer Research · Internal Medicine

Altamente citadoNo
Abrir DOISci-HubOpen Access
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