S Liu, S-J Lin, G Li et al. PPARg vs TR4 in PCa and 21:3 R279–R300 Review metabolic diseases Differential roles of PPARg vs TR4 in prostate cancer and metabolic diseases Su Liu1,*, Shin-Jen Lin1,*, Gonghui Li3,*, Eungseok Kim4, Yei-Tsung Chen5, Dong-Rong Yang1, M H Eileen Tan2, Eu Leong Yong2 and Chawnshang Chang1,6 1George Whipple Laboratory for Cancer Research, Departments of Pathology, Urology, Radiation Oncology, and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York 14642, USA 2Department of Obstetrics and Gynecology, National University of Singapore, Singapore, Singapore 3Chawnshang Chang Liver Cancer Center and Department of Urology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou 310016, China 4Department of Biological Sciences, Chonnam National University, Youngbong, Buk-Gu, Gwangju 500-757 Korea Correspondence 5Cardiovascular Research Institute, National University Health System and The Department of Medicine, should be addressed Yong Loo Lin School of Medicine, National University of Singapore, Singapore to C Chang 6Sex Hormone Research Center, China Medical University/Hospital, Taichung 404, Taiwan Email *(S Liu, S-J Lin and G Li are co-first authors)
[email protected] Abstract Peroxisome proliferator-activated receptor g (PPARg, NR1C3) and testicular receptor 4 Key Words nuclear receptor (TR4, NR2C2) are two members of the nuclear receptor (NR) superfamily " prostate that can be activated by several similar ligands/activators including polyunsaturated fatty " molecular genetics acid metabolites, such as 13-hydroxyoctadecadienoic acid and 15-hydroxyeicosatetraenoic Endocrine-Related Cancer acid, as well as some anti-diabetic drugs such as thiazolidinediones (TZDs). However, the consequences of the transactivation of these ligands/activators via these two NRs are different, with at least three distinct phenotypes.