Expression of Peroxisome Proliferator Activated Receptor gamma in Prostatic Adenocarcinoma.
Peroxisome proliferator-activated receptor gamma (PPAR-γ), a ligand-activated transcription factor has been investigated as the target for cancer treatment as well as metabolic disorders. Recent studies have demonstrated that PPAR-γ ligands are anti-tumorigenic in prostate cancer due to anti-proliferative and pro-differentiation effects. The aim of this study was to validate PPAR-γ expression in malignant and benign prostate tissues by immunohistochemistry and quantitative real-time polymerase chain reaction (PCR). A total of 730 prostatic adenocarcinomas (PCAs) including 63 whole sections from radical prostatectomy specimens and tissue microarrays containing 667 PCAs were subject to immunostaining for two PPAR-γ antibodies. Twenty-five benign prostate tissues and PCAs were selected for investigating mRNA expression by quantitative real-time PCR. 10.7% of PCAs (78/730) showed cytoplasmic immunoreactivity of PPAR-γ and no nuclear immunoreactivity was noted in PCAs. Most benign prostatic glands showed negative immunoreactivity of PPAR-γ except for variable weak cytoplasmic staining in some glands. Nuclear immunoreactivity of PPAR-γ was noted some central zone and verumontanum mucosal epithelium. The constitutive PPAR-γ mRNA showed significantly lower level in PCAs compared to that in the benign tissues. There was no difference of PPAR-γ mRNA expression between low (≤7) and high (>7) Gleason score groups. There was no association of PPAR-γ mRNA level or cytoplasmic immunostaining with Gleason grade or pathologic stage. Our study supported the evidence of extra-nuclear localization and nongenomic actions of PPAR-γ. Further studies are needed to assess the functional role of PPAR-γ and to validate its therapeutic implication in prostate cancer.
Department of Pathology, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul, Korea.
Hyung Kyu
0000-0002-5972-3516
HK
Park
Department of Pathology, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul, Korea.
HyunKyung
0000-0002-2528-6231
H
Kim
Department of Urology, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul, Korea.
Hyeong-Gon
0000-0002-5034-5299
HG
Kim
Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Young Mee
0000-0001-8766-2602
YM
Cho
Department of Pathology, International St. Mary's Hospital, Incheon, Korea.
Woon Yong
0000-0003-4786-2823
WY
Jung
Department of Pathology, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul, Korea.
Hye Seung
0000-0002-3591-9995
HS
Han
Department of Pathology, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul, Korea.
Tae Sook
0000-0002-3602-9257
TS
Hwang
Department of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Ghee Young
0000-0002-3304-577X
GY
Kwon
Department of Pathology, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul, Korea.
So Dug
0000-0003-2036-0313
SD
Lim
D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D047495:PPAR gamma / Q000235:genetics* / Q000378:metabolism*; D011467:Prostate / Q000473:pathology; D011468:Prostatectomy; D011471:Prostatic Neoplasms / Q000378:metabolism / Q000473:pathology*; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D046888:Tissue Array Analysis
D047495:PPAR gamma; D012333:RNA, Messenger
Immunohistochemistry; PPAR gamma; Prostatic Neoplasms; Real-Time Polymerase Chain Reaction