دورية أكاديمية

The Interleukin (IL)-1R1 pathway is a critical negative regulator of PyMT-mediated mammary tumorigenesis and pulmonary metastasis

التفاصيل البيبلوغرافية
العنوان: The Interleukin (IL)-1R1 pathway is a critical negative regulator of PyMT-mediated mammary tumorigenesis and pulmonary metastasis
المؤلفون: Maryse Dagenais, Jeremy Dupaul-Chicoine, Todd Douglas, Claudia Champagne, Alexandre Morizot, Maya Saleh
المصدر: OncoImmunology, Vol 6, Iss 3 (2017)
بيانات النشر: Taylor & Francis Group, 2017.
سنة النشر: 2017
المجموعة: LCC:Immunologic diseases. Allergy
LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
مصطلحات موضوعية: breast cancer, il-1r1, il-1α, inflammation, inflammasome, proliferation, tumor suppression, Immunologic diseases. Allergy, RC581-607, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
الوصف: Breast cancer is the most common cancer in women and the second leading cause of female cancer-related deaths worldwide. Inflammation is an established hallmark of tumorigenesis and an important determinant of tumor outcome and response to therapy. With advances in cancer immunotherapy, there is an urgent need to dissect the contribution of specific immune effectors in cancer development. Here, we genetically investigated the role of the Interleukin-1 (IL-1) receptor 1 (IL-1R1) pathway in breast cancer tumorigenesis and metastasis using the MMTV-PyMT mouse model. Our results indicate that IL-1R1 signaling suppresses mammary tumor cell proliferation early in tumorigenesis and curbs breast cancer outgrowth and pulmonary metastasis. We show that PyMT/Il1r1−/− mice had a higher primary tumor burden and increased mortality rate compared with IL-1R1-sufficient PyMT control mice. This phenotype was independent of the inflammatory caspases-1/-11 but driven by IL-1α, as PyMT/Il1a−/− mice phenocopied PyMT/Il1r1−/− mice. Collectively, our results suggest that IL-1α-mediated IL-1R1 signaling is tumor-suppressive in PyMT-driven breast cancer.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2162-402X
2162402X
Relation: https://doaj.org/toc/2162-402X
DOI: 10.1080/2162402X.2017.1287247
URL الوصول: https://doaj.org/article/3b928718ae344df5ae7b6a1871ef1169
رقم الأكسشن: edsdoj.3b928718ae344df5ae7b6a1871ef1169
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:2162402X
DOI:10.1080/2162402X.2017.1287247