Excavatolide B inhibits nonsmall cell lung cancer proliferation by altering peroxisome proliferator activated receptor gamma expression and PTEN/AKT/NF-Kβ expression

2016 ◽  
Vol 32 (1) ◽  
pp. 290-301 ◽  
Author(s):  
Bharath Kumar Velmurugan ◽  
Hsueh-Hui Yang ◽  
Ping-Jyun Sung ◽  
Ching-Feng Weng
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Nonsmall Cell Lung Cancer ◽  
Peroxisome Proliferator ◽  
Cancer Proliferation ◽  
Peroxisome Proliferator Activated Receptor

scholarly journals Peroxisome proliferator-activated receptor-γ activation inhibits tumor progression in non-small-cell lung cancer

Oncogene ◽  
2004 ◽  
Vol 23 (1) ◽  
pp. 100-108 ◽  
Author(s):  
Venkateshwar G Keshamouni ◽  
Raju C Reddy ◽  
Douglas A Arenberg ◽  
Binju Joel ◽  
Victor J Thannickal ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Tumor Progression ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Peroxisome Proliferator ◽  
Small Cell Lung ◽  
Peroxisome Proliferator Activated Receptor

scholarly journals Activation and Molecular Targets of Peroxisome Proliferator-Activated Receptor-γLigands in Lung Cancer

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
Raphael A. Nemenoff ◽  
Mary Weiser-Evans ◽  
Robert A. Winn
Keyword(s):  
Lung Cancer ◽  
Treatment Strategies ◽  
Nonsmall Cell Lung Cancer ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Treatment And Prevention ◽  
Direct Binding ◽  
Xenograft Models ◽  
New Treatment

Lung cancer is the leading cause of cancer death, and five-year survival remains poor, raising the urgency for new treatment strategies. Activation of PPARγrepresents a potential target for both the treatment and prevention of lung cancer. Numerous studies have examined the effect of thiazolidinediones such as rosiglitazone and pioglitazone on lung cancer cells in vitro and in xenograft models. These studies indicate that activation of PPARγinhibits cancer cell proliferation as well as invasiveness and metastasis. While activation of PPARγcan occur by direct binding of pharmacological ligands to the molecule, emerging data indicate that PPARγactivation can occur through engagement of other signal transduction pathways, including Wnt signaling and prostaglandin production. Data, both from preclinical models and retrospective clinical studies, indicate that activation of PPARγmay represent an attractive chemopreventive strategy. This article reviews the existing biological and mechanistic experiments focusing on the role of PPARγin lung cancer, focusing specifically on nonsmall cell lung cancer.

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