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The Scientific World Journal
Volume 2013, Article ID 607524, 5 pages
Research Article

Transcriptional Regulation of Δ6-Desaturase by Peroxisome Proliferative-Activated Receptor δ Agonist in Human Pancreatic Cancer Cells: Role of MEK/ERK1/2 Pathway

1Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz 5165665811, Iran
2Department of Clinical Biochemistry and Genetics, Cellular and Molecular Research Center, Faculty of Medicine, Qazvin University of Medical Sciences, Qazvin 3411975981, Iran
3Department of Anatomy and Cell Biology, Shahid Beheshti University of Medical Sciences, Tehran 193954719, Iran
4Department of Biotechnology, Cellular and Molecular and Burns Research Centers, Iran University of Medical Sciences, Tehran 141556183, Iran

Received 1 August 2013; Accepted 26 September 2013

Academic Editors: J. Mazella, A. Mentese, and B. Sharma

Copyright © 2013 Maryam Darabi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The Δ6-desaturase (Δ6D), also known as fatty acid desaturase 2, is a regulatory enzyme in de novo fatty acid synthesis, which has been linked to obesity and diabetes. The aim of the present study was to investigate the effect of peroxisome proliferative-activated receptor δ (PPARδ) agonist and MEK/ERK1/2-dependent pathway on the expression of Δ6D in human pancreatic carcinoma cell line PANC-1. PANC-1 cells cultured in RPMI-1640 were exposed to the commonly used ERK1/2 pathway inhibitor PD98059 and PPARδ agonist GW0742. Changes in mRNA and protein expression of Δ6D were then determined using real-time RT-PCR and Western blot, respectively. The expression of Δ6D ( ) increased following treatment with PPARδ agonist both at mRNA and protein levels, whereas no significant change was observed after treatment with MEK/ERK1/2 pathway inhibitor. It was also found that the increase in the expression of Δ6D in response to GW0742 was significantly inhibited by PD98059 (>40%, ) or EGF receptor-selective inhibitor AG1478 (>25%, ) pretreatment. PPARδ and MEK/ERK1/2 signaling pathways affect differentially the expression of Δ6D in pancreatic cancer cells. Furthermore, there may be an inhibitory crosstalk between these two regulatory pathways on the mRNA expression of Δ6D and subsequently on Δ6D protein expression.