Expression of peroxisome proliferator-activated receptor (PPAR) in human prostate cancer

Expression of peroxisome proliferator-activated receptor (PPAR) in human prostate cancer
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DOI:
10.1002/pros.10058
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发表时间:
2002-05-01
期刊:
影响因子:
2.8
通讯作者:
Sano, H
Sano, H
中科院分区:
医学3区
文献类型:
--
作者:
Segawa, Y;Yoshimura, R;Sano, H

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背景资料。最近的研究表明,过氧化体增殖物激活受体(PPAR)-γ在乳腺癌、肺癌、胃癌等癌细胞中均有表达,其配体通过凋亡诱导这些癌细胞的生长停滞。然而,PPAR在前列腺中的表达和定位还没有被研究过。方法收集156例前列腺癌(PC)、15例前列腺癌(PIN)、20例良性前列腺增生症(BPH)和12例正常前列腺(NP)组织,检测PPAR在前列腺癌(PC)、前列腺上皮内瘤(PIN)、良性前列腺增生症(BPH)和正常前列腺(NP)组织中的表达。结果:PPAR-α和PPAR-β在PC组织中呈明显阳性表达。PIN组、BPH组和NP组PPAR-α和-β也有明显表达。而PPAR-γ在BPH和NP中的表达很弱或不表达。PPAR-γ在PC组和PIN组的癌细胞中均有显著表达。结论PPAR-γ在PC中被诱导表达,提示PPAR-γ配体可能通过分化介导其自身对PC细胞的抗增殖作用。(C)2002年Wiley-Liss,Inc.
BACKGROUND. Recent studies have demonstrated that peroxisome proliferator activator-receptors (PPAR)-gamma is expressed in some cancer cells such as breast, lung, and gastric cancer, and its ligand induces growth arrest of these cancer cells through apoptosis. However, the expression and localization of PPARs in prostate have not been examined. In this study, PPARs expression was investigated in human prostate cancer (PC) prostatic intraepithelial neoplasia (PIN), benign prostatic hyperplasia (BPH), and normal prostate (NP) tissues.METHODS. Tumor specimens were obtained from 156 patients with PC, 15 with PIN, 20 with BPH, and 12 patients with NP tissues. The expressions were investigated by RT-PCR and immunohistochemical methods.RESULTS. Immunoreactive PPAR-alpha and -beta were significantly apparent in PC tissues. Marked expressions of PPAR-alpha, and -beta were also detected in PIN, BPH, and NP groups. However, very weak or no expression of immunoreactive PPAR-gamma was found in BPH and NP cases. In contrast, we found significant expression of immunoreactive PPAR-gamma in cancer cells in PC group and in PIN group.CONCLUSIONS. Our results demonstrated that PPAR-gamma is induced in PC, and suggest that PPAR-gamma ligands may mediate its own potent antiproliferative effect against PC cells through differentiation. (C) 2002 Wiley-Liss, Inc.