Global gene analysis identifying genes commonly regulated by the Ras/Raf/MEK and type I IFN pathways

Oncolytic viruses exploit alterations in cancer cells to specifically infect cancer cells but not normal healthy cells. Previous work has shown that oncogenic Ras interferes with interferon (IFN) signaling to promote viral replication. Furthermore, inhibition of the Ras/Raf/MEK/ERK pathway at the le...

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Main Authors: Y. Komatsu, K. Hirasawa, S.L. Christian
Format: Article
Language:English
Published: Elsevier 2015-06-01
Series:Genomics Data
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S221359601500029X
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author Y. Komatsu
K. Hirasawa
S.L. Christian
author_facet Y. Komatsu
K. Hirasawa
S.L. Christian
author_sort Y. Komatsu
collection DOAJ
description Oncolytic viruses exploit alterations in cancer cells to specifically infect cancer cells but not normal healthy cells. Previous work has shown that oncogenic Ras interferes with interferon (IFN) signaling to promote viral replication. Furthermore, inhibition of the Ras/Raf/MEK/ERK pathway at the level of Ras, MEK, or ERK was sufficient to restore IFN signaling. In order to identify genes that were commonly regulated by the inhibition of the Ras pathway and the IFN pathway, we treated NIH/3T3 cells that overexpress oncogenic Ras with the MEK inhibitor, U0126, or IFN-α for 6 h, and performed DNA microarray analysis (Gene Expression Omnibus accession number GSE49469). Here, we also provide additional information on the experimental and functional analysis of the genes responsive to U0126 and IFN.
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spelling doaj.art-79ee981ae38e49f7a0719091a4d449aa2022-12-22T01:59:02ZengElsevierGenomics Data2213-59602015-06-014C848710.1016/j.gdata.2015.03.012Global gene analysis identifying genes commonly regulated by the Ras/Raf/MEK and type I IFN pathwaysY. Komatsu0K. Hirasawa1S.L. Christian2Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, CanadaDivision of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, CanadaDivision of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, CanadaOncolytic viruses exploit alterations in cancer cells to specifically infect cancer cells but not normal healthy cells. Previous work has shown that oncogenic Ras interferes with interferon (IFN) signaling to promote viral replication. Furthermore, inhibition of the Ras/Raf/MEK/ERK pathway at the level of Ras, MEK, or ERK was sufficient to restore IFN signaling. In order to identify genes that were commonly regulated by the inhibition of the Ras pathway and the IFN pathway, we treated NIH/3T3 cells that overexpress oncogenic Ras with the MEK inhibitor, U0126, or IFN-α for 6 h, and performed DNA microarray analysis (Gene Expression Omnibus accession number GSE49469). Here, we also provide additional information on the experimental and functional analysis of the genes responsive to U0126 and IFN.http://www.sciencedirect.com/science/article/pii/S221359601500029XOncogenic RasRas/Raf/MEKU0126Type I interferonNIH/3T3
spellingShingle Y. Komatsu
K. Hirasawa
S.L. Christian
Global gene analysis identifying genes commonly regulated by the Ras/Raf/MEK and type I IFN pathways
Genomics Data
Oncogenic Ras
Ras/Raf/MEK
U0126
Type I interferon
NIH/3T3
title Global gene analysis identifying genes commonly regulated by the Ras/Raf/MEK and type I IFN pathways
title_full Global gene analysis identifying genes commonly regulated by the Ras/Raf/MEK and type I IFN pathways
title_fullStr Global gene analysis identifying genes commonly regulated by the Ras/Raf/MEK and type I IFN pathways
title_full_unstemmed Global gene analysis identifying genes commonly regulated by the Ras/Raf/MEK and type I IFN pathways
title_short Global gene analysis identifying genes commonly regulated by the Ras/Raf/MEK and type I IFN pathways
title_sort global gene analysis identifying genes commonly regulated by the ras raf mek and type i ifn pathways
topic Oncogenic Ras
Ras/Raf/MEK
U0126
Type I interferon
NIH/3T3
url http://www.sciencedirect.com/science/article/pii/S221359601500029X
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