Cytotoxicity of troglitazone through PPARγ-independent pathway and p38 MAPK pathway in renal cell carcinoma - Abstract

Department of Clinical Pharmacy, School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, 11-68 Koshien-kyuban-cho, Nishinomiya, Hyogo 663-8179, Japan.

 

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 G2/M cell cycle arrest through activation of p38 MAPK.

Written by:
Fujita M, Yagami T, Fujio M, Tohji C, Takase K, Yamamoto Y, Sawada K, Yamamori M, Okamura N.   Are you the author?

Reference: Cancer Lett. 2011 Dec 22;312(2):219-27.
doi: 10.1016/j.canlet.2011.08.010

PubMed Abstract
PMID: 21903322

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