曲格列酮通过 PPARγ 非依赖性通路和 p38MAPK 通路对肾癌细胞的细胞毒性作用。
Cytotoxicity of troglitazone through PPARγ-independent pathway and p38 MAPK pathway in renal cell carcinoma.
机构信息
Department of Clinical Pharmacy, School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Nishinomiya, Hyogo, Japan.
出版信息
Cancer Lett. 2011 Dec 22;312(2):219-27. doi: 10.1016/j.canlet.2011.08.010. Epub 2011 Aug 22.
Agonists of peroxisome proliferator-activated receptor gamma (PPARγ) have been examined as chemopreventive and chemotherapeutic agents. The aim was to investigate the cytotoxicity of troglitazone (TGZ) and its mechanisms in terms of PPARγ 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 PPARγ-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.
过氧化物酶体增殖物激活受体 γ（PPARγ）激动剂已被研究作为化学预防和化学治疗剂。本研究旨在探讨曲格列酮（TGZ）在三种人肾癌细胞系（786-O、Caki-2 和 ACHN 细胞）中的细胞毒性及其与 PPARγ 依赖性和 p38 丝裂原活化蛋白激酶（MAPK）通路的关系。TGZ 诱导细胞凋亡，并以非依赖于 PPARγ 的方式发挥细胞毒性。我们证实，TGZ 激活 p38 MAPK 通路并参与 TGZ 的细胞毒性。还揭示了 TGZ 通过激活 p38 MAPK 诱导 G2/M 细胞周期停滞。
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