PPARγ2 functions as a tumor suppressor in a translational mouse model of human prostate cancer  

作　　者：Fu-Lu Dong Dong-Mei Liu Ting-Ting Lu Feng Li Chong Zhang Qun E Yong-Hui Zhang 

机构地区：[1]Laboratory of Nuclear Receptors and Cancer Research,Department of Pathology,Medical School,Nantong University,Nantong 226001,China

出　　处：《Asian Journal of Andrology》2022年第1期90-96,共7页亚洲男性学杂志（英文版）

基　　金：The work was supported by the National Natural Science Foundation of China(NSFC;No.81874171 and 81703259).

摘　　要：Peroxisome proliferator-activated receptorsγ(PPARγ)is a master regulator that controls energy metabolism and cell fate.PPARγ2,a PPARγisoform,is highly expressed in the normal prostate but expressed at lower levels in prostate cancer tissues.In the present study,PC3 and LNCaP cells were used to examine the benefits of restoring PPARγ2 activity.PPARγ2 was overexpressed in PC3 and LNCaP cells,and cell proliferation and migration were detected.Hematoxylin and eosin(H&E)staining was used to detect pathological changes.The genes regulated by PPARγ2 overexpression were detected by microarray analysis.The restoration of PPARγ2 in PC3 and LNCaP cells inhibited cell proliferation and migration.PC3-PPARγ2 tissue recombinants showed necrosis in cancerous regions and leukocyte infiltration in the surrounding stroma by H&E staining.We found higher mixed lineage kinase domain-like(MLKL)and lower microtubule-associated protein 1 light chain 3(LC3)expression in cancer tissues compared to controls by immunohistochemistry(IHC)staining.Microarray analysis showed that PPARγ2 gain of function in PC3 cells resulted in the reprogramming of lipid-and energy metabolism-associated signaling pathways.These data indicate that PPARγ2 exerts a crucial tumor-suppressive effect by triggering necrosis and an inflammatory reaction in human prostate cancer.

关 键 词：inflammatory reaction NECROSIS PPARΓ prostate cancer tissue recombination-xenografting 

分 类 号：R737.25[医药卫生—肿瘤]