Chemical genomic-based pathway analyses for epidermal growth factor-mediated signaling in migrating cancer cells.

To explore the diversity and consistency of the signaling pathways that regulate tumor cell migration, we chose three human tumor cell lines that migrated after treatment with EGF. We then quantified the effect of fifteen inhibitors on the levels of expression or the phosphorylation levels of nine p...

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Main Authors: Shigeyuki Magi, Yuya Saeki, Masato Kasamatsu, Etsu Tashiro, Masaya Imoto
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4018296?pdf=render
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spelling doaj-74cfe664c4034a4a8dbd28a051610b532020-11-24T21:50:38ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0195e9677610.1371/journal.pone.0096776Chemical genomic-based pathway analyses for epidermal growth factor-mediated signaling in migrating cancer cells.Shigeyuki MagiYuya SaekiMasato KasamatsuEtsu TashiroMasaya ImotoTo explore the diversity and consistency of the signaling pathways that regulate tumor cell migration, we chose three human tumor cell lines that migrated after treatment with EGF. We then quantified the effect of fifteen inhibitors on the levels of expression or the phosphorylation levels of nine proteins that were induced by EGF stimulation in each of these cell lines. Based on the data obtained in this study and chemical-biological assumptions, we deduced cell migration pathways in each tumor cell line, and then compared them. As a result, we found that both the MEK/ERK and JNK/c-Jun pathways were activated in all three migrating cell lines. Moreover, GSK-3 and p38 were found to regulate PI3K/Akt pathway in only EC109 cells, and JNK was found to crosstalk with p38 and Fos related pathway in only TT cells. Taken together, our analytical system could easily distinguish between the common and cell type-specific pathways responsible for tumor cell migration.http://europepmc.org/articles/PMC4018296?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Shigeyuki Magi
Yuya Saeki
Masato Kasamatsu
Etsu Tashiro
Masaya Imoto
spellingShingle Shigeyuki Magi
Yuya Saeki
Masato Kasamatsu
Etsu Tashiro
Masaya Imoto
Chemical genomic-based pathway analyses for epidermal growth factor-mediated signaling in migrating cancer cells.
PLoS ONE
author_facet Shigeyuki Magi
Yuya Saeki
Masato Kasamatsu
Etsu Tashiro
Masaya Imoto
author_sort Shigeyuki Magi
title Chemical genomic-based pathway analyses for epidermal growth factor-mediated signaling in migrating cancer cells.
title_short Chemical genomic-based pathway analyses for epidermal growth factor-mediated signaling in migrating cancer cells.
title_full Chemical genomic-based pathway analyses for epidermal growth factor-mediated signaling in migrating cancer cells.
title_fullStr Chemical genomic-based pathway analyses for epidermal growth factor-mediated signaling in migrating cancer cells.
title_full_unstemmed Chemical genomic-based pathway analyses for epidermal growth factor-mediated signaling in migrating cancer cells.
title_sort chemical genomic-based pathway analyses for epidermal growth factor-mediated signaling in migrating cancer cells.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2014-01-01
description To explore the diversity and consistency of the signaling pathways that regulate tumor cell migration, we chose three human tumor cell lines that migrated after treatment with EGF. We then quantified the effect of fifteen inhibitors on the levels of expression or the phosphorylation levels of nine proteins that were induced by EGF stimulation in each of these cell lines. Based on the data obtained in this study and chemical-biological assumptions, we deduced cell migration pathways in each tumor cell line, and then compared them. As a result, we found that both the MEK/ERK and JNK/c-Jun pathways were activated in all three migrating cell lines. Moreover, GSK-3 and p38 were found to regulate PI3K/Akt pathway in only EC109 cells, and JNK was found to crosstalk with p38 and Fos related pathway in only TT cells. Taken together, our analytical system could easily distinguish between the common and cell type-specific pathways responsible for tumor cell migration.
url http://europepmc.org/articles/PMC4018296?pdf=render
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