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Plos One : Cell Survival Signalling Through Ppard and Arachidonic Acid Metabolites in Neuroblastoma, Volume 8

By Fei, Peiwen

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Book Id: WPLBN0003944993
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos One : Cell Survival Signalling Through Ppard and Arachidonic Acid Metabolites in Neuroblastoma, Volume 8  
Author: Fei, Peiwen
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection (Contemporary)
Historic
Publication Date:
Publisher: Plos

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Fei, P. (n.d.). Plos One : Cell Survival Signalling Through Ppard and Arachidonic Acid Metabolites in Neuroblastoma, Volume 8. Retrieved from http://netlibrary.net/


Description
Description : Retinoic acid (RA) has paradoxical effects on cancer cells : promoting cell death, differentiation and cell cycle arrest, or cell survival and proliferation. Arachidonic acid (AA) release occurs in response to RA treatment and, therefore, AA and its downstream metabolites may be involved in cell survival signalling. To test this, we inhibited phospholipase A2-mediated AA release, cyclooxygenases and lipoxygenases with small-molecule inhibitors to determine if this would sensitise cells to cell death after RA treatment. The data suggest that, in response to RA, phospholipase A2-mediated release of AA and subsequent metabolism by lipoxygenases is important for cell survival. Evidence from gene expression reporter assays and PPARd knockdown suggests that lipoxygenase metabolites activate PPARd. The involvement of PPARd in cell survival is supported by results of experiments with the PPARd inhibitor GSK0660 and siRNA-mediated knockdown. Quantitative reverse transcriptase PCR studies demonstrated that inhibition of 5-lipoxygenase after RA treatment resulted in a strong upregulation of mRNA for PPARd2, a putative inhibitory PPARd isoform. Over-expression of PPARd2 using a tetracyclineinducible system in neuroblastoma cells reduced proliferation and induced cell death. These data provide evidence linking lipoxygenases and PPARd in a cell survival-signalling mechanism and suggest new drug-development targets for malignant and hyper-proliferative diseases.

 

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