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Forum on Immunopathological Diseases and Therapeutics
SJR: 0.309 SNIP: 0.041 CiteScore™: 0.18

ISSN Imprimer: 2151-8017
ISSN En ligne: 2151-8025

Archives: Volume 1, 2010 to Volume 7, 2016

Forum on Immunopathological Diseases and Therapeutics

DOI: 10.1615/ForumImmunDisTher.2012006108
pages 117-124

S-Nitrosation Mediates Multiple Pathways That Lead to Tumor Progression in Estrogen Receptor−Negative Breast Cancer

Christopher H. Switzer
Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
Lisa A. Ridnour
Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
Robert Cheng
Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
Julie Heinecke
Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
Amy Burke
Prostate Cancer Institute, National University of Ireland Galway, Galway, Ireland
Sharon Glynn
Prostate Cancer Institute, National University of Ireland Galway, Galway, Ireland
Stefan Ambs
laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
David A. Wink
Cancer and Inflammation Program, National Cancer Institute-Frederick, Frederick, Maryland, USA

RÉSUMÉ

Chronic inflammation within the tumor microenvironment is a major driver of tumor progression and poor prognosis. Inducible nitric oxide synthase (NOS2) is present in numerous solid tumors. Estrogen receptor−negative (ER-) patients with high expression of tumor NOS2 have a poorer outcome than patients with low expression of NOS2. Furthermore, expression of NOS2 is associated with the basal-like breast cancer phenotype. Using an in vitro model, we have found that nitrosation of critical thiols and nitration of tyrosines lead to the activation of membrane receptors such as epithelial growth factor receptor, Src, Ras, and CD63. These nitric oxide−mediated events in itiate oncogenic signaling pathways such as PI3K/Akt, Ras/ERK, β-catenin, nuclear factor-κÂ, and AP-1. These data suggest that NOS2 can serve as a major "nonmutatational driver" of ER- breast cancer.


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