High AHR expression in breast tumors correlates with expression of genes from several signaling pathways namely inflammation and endogenous tryptophan metabolism

التفاصيل البيبلوغرافية
العنوان: High AHR expression in breast tumors correlates with expression of genes from several signaling pathways namely inflammation and endogenous tryptophan metabolism
المؤلفون: Ivan Bièche, Didier Meseure, François Lallemand, Martine Perrot-Applanat, Marc Pocard, Sophie Vacher, Patrice Castagnet, Walid Chemlali
المصدر: PLoS ONE
PLoS ONE, Vol 13, Iss 1, p e0190619 (2018)
بيانات النشر: Public Library of Science, 2018.
سنة النشر: 2018
مصطلحات موضوعية: 0301 basic medicine, Carcinogenesis, lcsh:Medicine, Gene Expression, Immunostaining, medicine.disease_cause, Pathology and Laboratory Medicine, Biochemistry, 0302 clinical medicine, Breast Tumors, Medicine and Health Sciences, lcsh:Science, Immune Response, Staining, Aged, 80 and over, Multidisciplinary, Tryptophan, respiratory system, Middle Aged, 3. Good health, Oncology, 030220 oncology & carcinogenesis, Tumor necrosis factor alpha, Female, Metabolic Pathways, Signal transduction, Anatomy, Research Article, Signal Transduction, Adult, Aryl hydrocarbon receptor nuclear translocator, Histology, Immunology, Breast Neoplasms, Biology, Research and Analysis Methods, Real-Time Polymerase Chain Reaction, 03 medical and health sciences, Signs and Symptoms, Diagnostic Medicine, Cell Line, Tumor, Breast Cancer, medicine, Genetics, Humans, RNA, Messenger, Insulin-like growth factor 1 receptor, Aged, Inflammation, Tumor microenvironment, lcsh:R, Estrogen Receptor alpha, Cancers and Neoplasms, Biology and Life Sciences, Aryl hydrocarbon receptor, respiratory tract diseases, 030104 developmental biology, Metabolism, Receptors, Aryl Hydrocarbon, Specimen Preparation and Treatment, Cancer research, biology.protein, lcsh:Q, Estrogen receptor alpha
الوصف: Increasing epidemiological and animal experimental data provide substantial support for the role of aryl hydrocarbon receptor (AhR) in mammary tumorigenesis. The effects of AhR have been clearly demonstrated in rodent models of breast carcinogenesis and in several established human breast cancer cell lines following exposure to AhR ligands or AhR overexpression. However, relatively little is known about the role of AhR in human breast cancers. AhR has always been considered to be a regulator of toxic and carcinogenic responses to environmental contaminants such as TCDD (dioxin) and benzo[a]pyrene (BaP). The aim of this study was to identify the type of breast tumors (ERα-positive or ERα-negative) that express AHR and how AhR affects human tumorigenesis. The levels of AHR, AHR nuclear translocator (ARNT) and AHR repressor (AHRR) mRNA expression were analyzed in a cohort of 439 breast tumors, demonstrating a weak association between high AHR expression and age greater than fifty years and ERα-negative status, and HR-/ERBB2 breast cancer subtypes. AHRR mRNA expression was associated with metastasis-free survival, while AHR mRNA expression was not. Immunohistochemistry revealed the presence of AhR protein in both tumor cells (nucleus and/or cytoplasm) and the tumor microenvironment (including endothelial cells and lymphocytes). High AHR expression was correlated with high expression of several genes involved in signaling pathways related to inflammation (IL1B, IL6, TNF, IL8 and CXCR4), metabolism (IDO1 and TDO2 from the kynurenine pathway), invasion (MMP1, MMP2 and PLAU), and IGF signaling (IGF2R, IGF1R and TGFB1). Two well-known ligands for AHR (TCDD and BaP) induced mRNA expression of IL1B and IL6 in an ERα-negative breast tumor cell line. The breast cancer ER status likely influences AhR activity involved in these signaling pathways. The mechanisms involved in AhR activation and target gene expression in breast cancers are also discussed.
اللغة: English
تدمد: 1932-6203
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b7d283e486889cfdec14d91963721910Test
http://europepmc.org/articles/PMC5761880Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....b7d283e486889cfdec14d91963721910
قاعدة البيانات: OpenAIRE