Cytotoxicity of troglitazone through PPARγ-independent pathway and p38 MAPK pathway in renal cell carcinoma
Cytotoxicity of troglitazone through PPARγ-independent pathway and p38 MAPK pathway in renal cell carcinoma
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DOI：
10.1016/j.canlet.2011.08.010
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发表时间：
2011-12-22
期刊：
影响因子：
9.7
通讯作者：
Okamura, Noboru
中科院分区：
文献类型：
--
作者：
Fujita, Megumi;Yagami, Tatsurou;Okamura, Noboru
过氧化物酶体增殖物激活受体γ（PPARγ）的激动剂已被检验为化学预防剂和化疗剂。目的是研究曲格列酮 (TGZ) 在三种人肾细胞癌 (RCC) 细胞系 786-O、Caki-2 和 ACHN 细胞中的细胞毒性及其在 PPAR γ 依赖性和 p38 丝裂原激活蛋白激酶 (MAPK) 通路方面的机制。 TGZ 诱导细胞凋亡并以不依赖于 PPAR γ 的方式发挥细胞毒性。我们证明TGZ激活p38 MAPK通路并参与TGZ的细胞毒性。研究还表明，TGZ 通过激活 p38 MAPK 诱导 G(2)/M 细胞周期停滞。 (C) 2011 Elsevier Ireland Ltd. 保留所有权利。
Agonists of peroxisome proliferator-activated receptor gamma (PPAR gamma) have been examined as chemopreventive and chemotherapeutic agents. The aim was to investigate the cytotoxicity of troglitazone (TGZ) and its mechanisms in terms of PPAR gamma dependency and the p38 mitogen-activated protein kinase (MAPK) pathway in three human renal cell carcinoma (RCC) cell lines, 786-O, Caki-2 and ACHN cells. TGZ induced apoptosis and exerted cytotoxicity in a PPAR gamma-independent manner. We demonstrated that TGZ activated the p38 MAPK pathway and was involved in the cytotoxicity of TGZ. It was also revealed that TGZ induced G(2)/M cell cycle arrest through activation of p38 MAPK. (C) 2011 Elsevier Ireland Ltd. All rights reserved.