Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARγ Dependent and Independent Mechanisms

Although thiazolidinediones (TZDs) were found to be ligands for peroxisome proliferators-activated receptorγ (PPARγ), the mechanism by which TZDs exert their anticancer effect remains unclear. Furthermore, the effect of TZDs on metastatic and angiogenesis potential of cancer cells is unknown. Our re...

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Main Authors: Qing He, Ruiping Pang, Xin Song, Jie Chen, Huixin Chen, Baili Chen, Pinjin Hu, Minhu Chen
Format: Article
Language:English
Published: Wiley 2008-01-01
Series:PPAR Research
Online Access:http://dx.doi.org/10.1155/2008/649808
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author Qing He
Ruiping Pang
Xin Song
Jie Chen
Huixin Chen
Baili Chen
Pinjin Hu
Minhu Chen
author_facet Qing He
Ruiping Pang
Xin Song
Jie Chen
Huixin Chen
Baili Chen
Pinjin Hu
Minhu Chen
author_sort Qing He
collection DOAJ
description Although thiazolidinediones (TZDs) were found to be ligands for peroxisome proliferators-activated receptorγ (PPARγ), the mechanism by which TZDs exert their anticancer effect remains unclear. Furthermore, the effect of TZDs on metastatic and angiogenesis potential of cancer cells is unknown. Our results in this paper show that rosiglitazone inhibited SGC-7901 gastric cancer cells growth, caused G1 cell cycle arrest and induced apoptosis in a dose-dependent manner. The effects of rosiglitazone on SGC-7901 cancer cells were completely reversed by treatment with PPARγ antagonist GW9662. Rosiglitazone inhibited SGC-7901 cell migration, invasiveness, and the expression of MMP-2 in dose-dependent manner via PPARγ-independent manner. Rosiglitazone reduced the VEGF induced angiogenesis of HUVEC in dose-dependent manner through PPARγ-dependent pathway. Moreover, rosiglitazone did not affect the expression of VEGF by SGC-7901 cells. Our results demonstrated that by PPARγ ligand, rosiglitazone inhibited growth and invasiveness of SGC-7901 gastric cancer cells and angiogenesis in vitro via PPARγ-dependent or -independent pathway.
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institution Kabale University
issn 1687-4757
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language English
publishDate 2008-01-01
publisher Wiley
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series PPAR Research
spelling doaj-art-09d33b7d4f464981a6ecd93c8f1b46432025-08-20T03:55:29ZengWileyPPAR Research1687-47571687-47652008-01-01200810.1155/2008/649808649808Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARγ Dependent and Independent MechanismsQing He0Ruiping Pang1Xin Song2Jie Chen3Huixin Chen4Baili Chen5Pinjin Hu6Minhu Chen7Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Physiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, ChinaDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, ChinaAlthough thiazolidinediones (TZDs) were found to be ligands for peroxisome proliferators-activated receptorγ (PPARγ), the mechanism by which TZDs exert their anticancer effect remains unclear. Furthermore, the effect of TZDs on metastatic and angiogenesis potential of cancer cells is unknown. Our results in this paper show that rosiglitazone inhibited SGC-7901 gastric cancer cells growth, caused G1 cell cycle arrest and induced apoptosis in a dose-dependent manner. The effects of rosiglitazone on SGC-7901 cancer cells were completely reversed by treatment with PPARγ antagonist GW9662. Rosiglitazone inhibited SGC-7901 cell migration, invasiveness, and the expression of MMP-2 in dose-dependent manner via PPARγ-independent manner. Rosiglitazone reduced the VEGF induced angiogenesis of HUVEC in dose-dependent manner through PPARγ-dependent pathway. Moreover, rosiglitazone did not affect the expression of VEGF by SGC-7901 cells. Our results demonstrated that by PPARγ ligand, rosiglitazone inhibited growth and invasiveness of SGC-7901 gastric cancer cells and angiogenesis in vitro via PPARγ-dependent or -independent pathway.http://dx.doi.org/10.1155/2008/649808
spellingShingle Qing He
Ruiping Pang
Xin Song
Jie Chen
Huixin Chen
Baili Chen
Pinjin Hu
Minhu Chen
Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARγ Dependent and Independent Mechanisms
PPAR Research
title Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARγ Dependent and Independent Mechanisms
title_full Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARγ Dependent and Independent Mechanisms
title_fullStr Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARγ Dependent and Independent Mechanisms
title_full_unstemmed Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARγ Dependent and Independent Mechanisms
title_short Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARγ Dependent and Independent Mechanisms
title_sort rosiglitazone suppresses the growth and invasiveness of sgc 7901 gastric cancer cells and angiogenesis in vitro via pparγ dependent and independent mechanisms
url http://dx.doi.org/10.1155/2008/649808
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