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Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation

Fos-related antigen 1 (Fra1) has been proposed as a gatekeeper of the mesenchymal-epithelial transition to epithelial-mesenchymal transition. Here, we showed that de-phosphorylated JNK2 increased the expression of Fra1 by promoting the expression of c-Jun and Jun-B. Conversely, phosphorylated JNK2 s...

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Autores principales: Hu, Sike, Dong, Xiaoli, Gao, Wenjuan, Stupack, Dwayne, Liu, Yanhua, Xiang, Rong, Li, Na
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5593584/
https://www.ncbi.nlm.nih.gov/pubmed/28915613
http://dx.doi.org/10.18632/oncotarget.17507
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author Hu, Sike
Dong, Xiaoli
Gao, Wenjuan
Stupack, Dwayne
Liu, Yanhua
Xiang, Rong
Li, Na
author_facet Hu, Sike
Dong, Xiaoli
Gao, Wenjuan
Stupack, Dwayne
Liu, Yanhua
Xiang, Rong
Li, Na
author_sort Hu, Sike
collection PubMed
description Fos-related antigen 1 (Fra1) has been proposed as a gatekeeper of the mesenchymal-epithelial transition to epithelial-mesenchymal transition. Here, we showed that de-phosphorylated JNK2 increased the expression of Fra1 by promoting the expression of c-Jun and Jun-B. Conversely, phosphorylated JNK2 suppressed its expression via enhancing the ubiquitination of c-Jun and Jun-B. These data provided insights into the regulatory mechanism of JNK2 on the expression of Fra1. Our study thus demonstrated that the conversion of JNK2 from its phosphorylation to de-phosphorylation status promoted the switch of breast cancer cells from mesenchymal-epithelial transition to epithelial-mesenchymal transition.
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spelling pubmed-55935842017-09-14 Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation Hu, Sike Dong, Xiaoli Gao, Wenjuan Stupack, Dwayne Liu, Yanhua Xiang, Rong Li, Na Oncotarget Research Paper Fos-related antigen 1 (Fra1) has been proposed as a gatekeeper of the mesenchymal-epithelial transition to epithelial-mesenchymal transition. Here, we showed that de-phosphorylated JNK2 increased the expression of Fra1 by promoting the expression of c-Jun and Jun-B. Conversely, phosphorylated JNK2 suppressed its expression via enhancing the ubiquitination of c-Jun and Jun-B. These data provided insights into the regulatory mechanism of JNK2 on the expression of Fra1. Our study thus demonstrated that the conversion of JNK2 from its phosphorylation to de-phosphorylation status promoted the switch of breast cancer cells from mesenchymal-epithelial transition to epithelial-mesenchymal transition. Impact Journals LLC 2017-04-28 /pmc/articles/PMC5593584/ /pubmed/28915613 http://dx.doi.org/10.18632/oncotarget.17507 Text en Copyright: © 2017 Hu et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Research Paper
Hu, Sike
Dong, Xiaoli
Gao, Wenjuan
Stupack, Dwayne
Liu, Yanhua
Xiang, Rong
Li, Na
Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation
title Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation
title_full Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation
title_fullStr Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation
title_full_unstemmed Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation
title_short Alternative promotion and suppression of metastasis by JNK2 governed by its phosphorylation
title_sort alternative promotion and suppression of metastasis by jnk2 governed by its phosphorylation
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5593584/
https://www.ncbi.nlm.nih.gov/pubmed/28915613
http://dx.doi.org/10.18632/oncotarget.17507
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