Thiazolidinediones enhance vascular endothelial growth factor expression and induce cell growth inhibition in non-small-cell lung cancer cells
It is known that thiazolidinediones are involved in regulating the expression of various genes, including the vascular endothelial growth factor (VEGF) gene via peroxisome proliferator-activated receptor gamma (PPARgamma); VEGF is a prognostic biomarker for non-small-cell lung cancer (NSCLC).
Methods: In this study, we investigated the effects of troglitazone on the mRNA expression of VEGF and its receptors in NSCLC cell lines RERF-LC-AI, SK-MES-1, PC-14, and A549. These mRNA expressions were evaluated by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis.
We also studied the effect of Je-11, a VEGF inhibitor, on the growth of these cells.
Results: In NSCLC cells, thiazolidinediones increased the mRNA expression of VEGF and neuropilin-1, but not that of other receptors such as fms-like tyrosine kinase and kinase insert domain receptor-1. Furthermore, the PPARgamma antagonist GW9662 completely reversed this thiazolidinedione-induced increase in VEGF expression.
Furthermore, the addition of VEGF inhibitors into the culture medium resulted in the reversal of thiazolidinedione-induced growth inhibition.
Conclusions: Our results indicated that thiazolidinediones enhance VEGF and neuropilin-1 expression and induce the inhibition of cell growth. We propose the existence of a pathway for arresting cell growth that involves the interaction of thiazolidinedione-induced VEGF and neuropilin-1 in NSCLC.
Author: Takayuki YoshizakiWataru MotomuraSachie TannoShima KumeiYumiko YoshizakiSatoshi TannoToshikatsu Okumura
Credits/Source: Journal of Experimental &Clinical Cancer Research 2010, 29:22
Published on: 2010-03-10
Copyright by the authors listed above - made available via BioMedCentral (Open Access). Please
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