Hijacking of the AP-1 Signaling Pathway during Development of ATL

Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T-cell leukemia (ATL). One way to address the pathology of the disease lies on conducting research with a molecular approach. In addition to the analysis of ATL-relevant signaling pathways, unders...

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Main Authors: Hélène Gazon, Benoit Barbeau, Jean-Michel Mesnard, Jean-Marie Peloponese
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-01-01
Series:Frontiers in Microbiology
Subjects:
Online Access:http://journal.frontiersin.org/article/10.3389/fmicb.2017.02686/full
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author Hélène Gazon
Benoit Barbeau
Jean-Michel Mesnard
Jean-Marie Peloponese
author_facet Hélène Gazon
Benoit Barbeau
Jean-Michel Mesnard
Jean-Marie Peloponese
author_sort Hélène Gazon
collection DOAJ
description Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T-cell leukemia (ATL). One way to address the pathology of the disease lies on conducting research with a molecular approach. In addition to the analysis of ATL-relevant signaling pathways, understanding the regulation of important and relevant transcription factors allows researchers to reach this fundamental objective. HTLV-1 encodes for two oncoproteins, Tax and HTLV-1 basic leucine-zipper factor, which play significant roles in the cellular transformation and the activation of the host’s immune responses. Activating protein-1 (AP-1) transcription factor has been linked to cancer and neoplastic transformation ever since the first representative members of the Jun and Fos gene family were cloned and shown to be cellular homologs of viral oncogenes. AP-1 is a dimeric transcription factor composed of proteins belonging to the Jun (c-Jun, JunB, and JunD), Fos (c-Fos, FosB, Fra1, and Fra2), and activating transcription factor protein families. Activation of AP-1 transcription factor family by different stimuli, such as inflammatory cytokines, stress inducers, or pathogens, results in innate and adaptive immunity. AP-1 is also involved in various cellular events including differentiation, proliferation, survival, and apoptosis. Deregulated expression of AP-1 transcription factors is implicated in various lymphomas such as classical Hodgkin lymphomas, anaplastic large cell lymphomas, diffuse large B-cell lymphomas, and adult T-cell leukemia. Here, we review the current thinking behind deregulation of the AP-1 pathway and its contribution to HTLV-induced cellular transformation.
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spelling doaj.art-59527e9fc2a14344926f88160fe9d25d2022-12-22T02:57:04ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2018-01-01810.3389/fmicb.2017.02686325600Hijacking of the AP-1 Signaling Pathway during Development of ATLHélène Gazon0Benoit Barbeau1Jean-Michel Mesnard2Jean-Marie Peloponese3Belgium Molecular and Cellular Epigenetics, Interdisciplinary Cluster for Applied Genoproteomics, University of Liège, Liège, BelgiumDépartement des Sciences Biologiques and Centre de Recherche BioMed, Université du Québec à Montréal, Montréal, QC, CanadaInstitut de Recherche en Infectiologie de Montpellier, Centre National de la Recherche Scientifique, Université de Montpellier, Montpellier, FranceInstitut de Recherche en Infectiologie de Montpellier, Centre National de la Recherche Scientifique, Université de Montpellier, Montpellier, FranceHuman T-cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T-cell leukemia (ATL). One way to address the pathology of the disease lies on conducting research with a molecular approach. In addition to the analysis of ATL-relevant signaling pathways, understanding the regulation of important and relevant transcription factors allows researchers to reach this fundamental objective. HTLV-1 encodes for two oncoproteins, Tax and HTLV-1 basic leucine-zipper factor, which play significant roles in the cellular transformation and the activation of the host’s immune responses. Activating protein-1 (AP-1) transcription factor has been linked to cancer and neoplastic transformation ever since the first representative members of the Jun and Fos gene family were cloned and shown to be cellular homologs of viral oncogenes. AP-1 is a dimeric transcription factor composed of proteins belonging to the Jun (c-Jun, JunB, and JunD), Fos (c-Fos, FosB, Fra1, and Fra2), and activating transcription factor protein families. Activation of AP-1 transcription factor family by different stimuli, such as inflammatory cytokines, stress inducers, or pathogens, results in innate and adaptive immunity. AP-1 is also involved in various cellular events including differentiation, proliferation, survival, and apoptosis. Deregulated expression of AP-1 transcription factors is implicated in various lymphomas such as classical Hodgkin lymphomas, anaplastic large cell lymphomas, diffuse large B-cell lymphomas, and adult T-cell leukemia. Here, we review the current thinking behind deregulation of the AP-1 pathway and its contribution to HTLV-induced cellular transformation.http://journal.frontiersin.org/article/10.3389/fmicb.2017.02686/fullAP-1HTLV-1antisense transcriptionleukemiaHBZJunD
spellingShingle Hélène Gazon
Benoit Barbeau
Jean-Michel Mesnard
Jean-Marie Peloponese
Hijacking of the AP-1 Signaling Pathway during Development of ATL
Frontiers in Microbiology
AP-1
HTLV-1
antisense transcription
leukemia
HBZ
JunD
title Hijacking of the AP-1 Signaling Pathway during Development of ATL
title_full Hijacking of the AP-1 Signaling Pathway during Development of ATL
title_fullStr Hijacking of the AP-1 Signaling Pathway during Development of ATL
title_full_unstemmed Hijacking of the AP-1 Signaling Pathway during Development of ATL
title_short Hijacking of the AP-1 Signaling Pathway during Development of ATL
title_sort hijacking of the ap 1 signaling pathway during development of atl
topic AP-1
HTLV-1
antisense transcription
leukemia
HBZ
JunD
url http://journal.frontiersin.org/article/10.3389/fmicb.2017.02686/full
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AT benoitbarbeau hijackingoftheap1signalingpathwayduringdevelopmentofatl
AT jeanmichelmesnard hijackingoftheap1signalingpathwayduringdevelopmentofatl
AT jeanmariepeloponese hijackingoftheap1signalingpathwayduringdevelopmentofatl