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


 Laboratory of Nuclear Receptors and Cancer Research, Department of Pathology, Medical School, Nantong University, Nantong 226001, China

Correspondence Address:
Yong-Hui Zhang,
Laboratory of Nuclear Receptors and Cancer Research, Department of Pathology, Medical School, Nantong University, Nantong 226001
China
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aja.aja_51_21

PMID: 34213488

Peroxisome proliferator-activated receptors γ (PPARγ) is a master regulator that controls energy metabolism and cell fate. PPARγ2, a PPARγ isoform, 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.


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    -  Dong FL
    -  Liu DM
    -  Lu TT
    -  Li F
    -  Zhang C
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