Inhibition of cell motility by troglitazone in human ovarian carcinoma cell line

Troglitazone (TGZ) is a potential anticancer agent. Little is known about the effect of this agent on cancer cell migration. Human ovarian carcinoma cell line, ES-2 cells were treated with various concentrations of TGZ. Cell migration was evaluated by wound-healing and Boyden chamber transwell exper...

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Published in:BMC cancer 2007-11, Vol.7 (1), p.216-216, Article 216
Main Authors: Yang, Yuh-Cheng, Ho, Tsung-Chuan, Chen, Show-Li, Lai, Huei-Yi, Wu, Ju-Yun, Tsao, Yeou-Ping
Format: Article
Language:English
Subjects:
Cell Line, Tumor
Cell Movement - drug effects
Cell Movement - physiology
Chromans - pharmacology
Chromans - therapeutic use
Dosage and administration
Dose-Response Relationship, Drug
Drug therapy
Female
Humans
Ovarian cancer
Ovarian Neoplasms - drug therapy
Ovarian Neoplasms - pathology
Thiazolidinediones - pharmacology
Thiazolidinediones - therapeutic use
Troglitazone
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Summary:Troglitazone (TGZ) is a potential anticancer agent. Little is known about the effect of this agent on cancer cell migration. Human ovarian carcinoma cell line, ES-2 cells were treated with various concentrations of TGZ. Cell migration was evaluated by wound-healing and Boyden chamber transwell experiments. PPARgamma expression was blocked by PPARgamma small interfering RNA. The effects of TGZ on phosphorylation of FAK, PTEN, Akt were assessed by immunoblotting using phospho-specific antibodies. The cellular distribution of paxillin, vinculin, stress fiber and PTEN was assessed by immunocytochemistry. TGZ dose- and time-dependently impaired cell migration through a PPARgamma independent manner. TGZ treatment impaired cell spreading, stress fiber formation, tyrosine phosphorylation of focal adhesion kinase (FAK), and focal adhesion assembly in cells grown on fibronectin substratum. TGZ also dose- and time-dependently suppressed FAK autophosphorylation and phosphorylation of the C-terminal of PTEN (a phosphatase). At concentration higher than 10 muM, TGZ caused accumulation of PTEN in plasma membrane, a sign of PTEN activation. These results indicate that TGZ can suppress cultured ES-2 cells migration. Our data suggest that the anti-migration potential of TGZ involves in regulations of FAK and PTEN activity.
ISSN:1471-2407
1471-2407
DOI:10.1186/1471-2407-7-216