题 目：Genetic dissection of the function of thyroid hormone receptors: from experimental approaches in the mouse to human pathology
报告人：Jacques Samarut 教授
主持人♛💇🏽♀️：翁杰敏 教授
时 间🤵🏽： 2015年10月22日下午15:00-15:30 （周四下午）
地 点：闵行校区天美娱乐534报告厅
报告人简介：Jacques Samarut got his PhD at the University of Lyon in 1982. He was then appointed as Associate Professor at the Rockefeller University of New York and then as Invited Professor at the Institute of Medical Science, University of Tokyo. He is presently professor of molecular biology at the Faculty of Medicine, Université Claude Bernard, Lyon. From 2008 to 2014 he has been the President of the Ecole Normale Supérieure de Lyon a prestigious graduate school. He had been formerly director of the Life Sciences study section of the French National Agency for Scientific Research (CNRS) and President of the scientific advisory board of the French National Institute for Agronomy (INRA). He received several awards including the Leukemia award of the French League against Cancer (1987) and the Rosen Award Foundation for Medical Research, Paris (1990), and the silver medal of the CNRS (1997) for his work on the role of oncogenes and nuclear receptors in oncogenic transformation. He is presently working on genomics of nuclear receptors. He published more than 160 original articles in international scientific journals. His research work generated several patents and contributed to the creation of two biotech companies (Genoway, Vivalis). He was honored as Chevalier de la Légion d’Honneur and Officier de l’Ordre National du Mérite. He is Doctor Honoris Causa of the University of Ottawa and Honorary Professor and Higher End Expert of the East China University of Shanghai.
报告内容简介：Androgen receptor (AR) is a ligand-dependent transcription factor. Upon activating by androgens, AR regulates gene transcription through binding to specific regulatory regions of target genes. In men, AR is essential for both sexual differentiation and prostate development. It is implicated in every steps of the prostate cancer, which is the most common cancer among men in Western countries. Androgens activate cell proliferation at the very early stages of tumor development. At some advanced stage of tumor progression leading to metastasis, androgen suppression therapy becomes inefficient and tumor development becomes independent of androgens. Escape of tumor growth from the control by androgens results from alterations in the function of the androgen receptor-signaling pathway. The molecular bases of these alterations are still poorly understood. In any case identifying downstream target genes of AR should help in understanding the mechanisms through which AR signaling might activate prostate tumor cell proliferation. In addition, it is likely that identifying some of these genes might provide helpful diagnostic and prognostic markers of prostate tumor development. We have identified several new AR target genes, among which some genes producing microRNA. We also identified a new way of regulation of some target genes by cooperative action of AR and the transcription factor E2F1 through chromatin looping in the regulatory region of these genes. Our aim is now to check whether some of these target genes might be prognostic markers for prostate tumor development. The molecular determinants of the functional interaction between E2F1 and AR are also investigated to open potential new ways of therapeutical approach.
