Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARgamma Dependent and Independent Mechanisms.
Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARgamma Dependent and Independent Mechanisms.
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Rosiglitazone 通过 PPARgamma 依赖性和独立机制抑制 SGC-7901 胃癌细胞的生长和侵袭以及体外血管生成。
DOI：
10.1155/2008/649808
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发表时间：
2008
期刊：
影响因子：
2.9
通讯作者：
Chen M
中科院分区：
文献类型：
--
作者：
He Q;Pang R;Song X;Chen J;Chen H;Chen B;Hu P;Chen M
噻唑烷二酮类化合物（TZDs）是过氧化物酶体增殖物激活受体γ（PPARγ）的配体，但TZDs发挥抗肿瘤作用的机制尚不清楚。此外，TZD对癌细胞的转移和血管生成潜力的影响尚不清楚。本实验结果表明罗格列酮对胃癌细胞株SGC-7901的生长有抑制作用，并呈剂量依赖性地使细胞周期阻滞于G1期，诱导细胞凋亡。罗格列酮对SGC-7901细胞的作用可被PPARγ拮抗剂GW 9662完全逆转。罗格列酮通过非依赖于PPARγ的方式抑制SGC-7901细胞的迁移、侵袭和MMP-2的表达，并呈剂量依赖性。罗格列酮通过PPARγ依赖性途径抑制VEGF诱导的HUVEC血管生成，且呈剂量依赖性。罗格列酮不影响胃癌细胞VEGF的表达。结果表明，罗格列酮通过PPARγ依赖或非依赖途径抑制胃癌细胞的生长、侵袭和血管生成。
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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