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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Frontiers Media S.A.
2018-01-01
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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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institution | Directory Open Access Journal |
issn | 1664-302X |
language | English |
last_indexed | 2024-04-13T07:03:08Z |
publishDate | 2018-01-01 |
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series | Frontiers in Microbiology |
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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