Expression of peroxisome proliferator-activated receptor γ in renal cell carcinoma and growth inhibition by its agonists

被引：91

作者：

Inoue, K ^{[1
]}

Kawahito, Y ^{[1
]}

Tsubouchi, Y ^{[1
]}

Kohno, M ^{[1
]}

Yoshimura, R ^{[1
]}

Yoshikawa, T ^{[1
]}

Sano, H ^{[1
]}

机构：

[1] Osaka City Univ, Sch Med, Dept Urol, Osaka 545, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2001年 / 287卷 / 03期

关键词：

peroxisome proliferator-activated receptor-gamma; renal cell carcinoma; immunohistochemistry; RT-PCR;

D O I：

10.1006/bbrc.2001.5640

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is a ligand-activated transcriptional factor belonging to the steroid receptor superfamily. It plays a role in both adipocyte differentiation and tumorgenesis. Up-date, the up-regulation of PPAR-gamma expression is a frequent occurrence in a variety of different malignant tumors. In this study, we investigated the expression of PPAR-gamma in human renal cell carcinoma (RCC tissues, and the role of PPAR-gamma in cell growth in human RCC-derived cell lines. Immunohistochemistry showed a strong immunoreactive expression of PPAR-gamma in all slides from cancer specimens. RT-PCR and Western blot analysis showed 3 RCC cell lines expressed PPAR-gamma mRNA and its protein. MTT assay in 3 RCC cells showed that the synthetic PPAR-gamma agonists thiazolidinedione compounds (pioglitazone and troglitazone) and the endogeneous PPAR-gamma ligand, 15-deoxy-Delta 12,14-prostaglandin J(2) (15dPGJ(2)) inhibited the growth of the RCC cells. These results suggest that PPAR-gamma may become a new target in the treatment of RCC. (C) 2001 Academic Press.

引用

页码：727 / 732

页数：6

共 25 条

[1] PPAR gamma induces cell cycle withdrawal: inhibition of E2F/DP DNA-binding activity via down-regulation of PP2A [J].