Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid Carcinoma

There is strong association between inflammatory processes and their main metabolic mediators, such as leptin, adiponectin secretion, and low/high-density lipoproteins, with the cancer risk and aggressive behavior of solid tumors. In this scenario, cancer cells (CCs) and cancer stem cells (CSCs) hav...

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Authors: Revilla, Giovanna|||0000-0003-2971-5651, Corcoy i Pla, Rosa|||0000-0001-5055-6814, Moral, Antonio|||0000-0001-5551-0145, Escolà-Gil, Joan Carles|||0000-0001-9021-2485, Mato, Eugènia|||0000-0001-8121-9335
Format: article
Publication Date:2019
Country:España
Institution:Universitat Autònoma de Barcelona
Repository:Dipòsit Digital de Documents de la UAB
Language:English
OAI Identifier:oai:ddd.uab.cat:253288
Online Access:https://ddd.uab.cat/record/253288
https://dx.doi.org/urn:doi:10.3390/ijms20102466
Access Level:Open access
Keyword:Thyroid carcinoma
Signaling pathways
MET/EMT
Leptin
Adiponectin
Low-density lipoproteins
High-density lipoproteins
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spelling Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid CarcinomaRevilla, Giovanna|||0000-0003-2971-5651Corcoy i Pla, Rosa|||0000-0001-5055-6814Moral, Antonio|||0000-0001-5551-0145Escolà-Gil, Joan Carles|||0000-0001-9021-2485Mato, Eugènia|||0000-0001-8121-9335Thyroid carcinomaSignaling pathwaysMET/EMTLeptinAdiponectinLow-density lipoproteinsHigh-density lipoproteinsThere is strong association between inflammatory processes and their main metabolic mediators, such as leptin, adiponectin secretion, and low/high-density lipoproteins, with the cancer risk and aggressive behavior of solid tumors. In this scenario, cancer cells (CCs) and cancer stem cells (CSCs) have important roles. These cellular populations, which come from differentiated cells and progenitor stem cells, have increased metabolic requirements when it comes to maintaining or expanding the tumors, and they serve as links to some inflammatory mediators. Although the molecular mechanisms that are involved in these associations remain unclear, the two following cellular pathways have been suggested: 1) the mesenchymal-epithelial transition (MET) process, which permits the differentiation of adult stem cells throughout the acquisition of cell polarity and the adhesion to epithelia, as well to new cellular lineages (CSCs); and, 2) a reverse process, termed the epithelial-mesenchymal transition (EMT), where, in pathophysiological conditions (tissue injury, inflammatory process, and oxidative stress), the differentiated cells can acquire a multipotent stem cell-like phenotype. The molecular mechanisms that regulate both EMT and MET are complex and poorly understood. Especially, in the thyroid gland, little is known regarding MET/EMT and the role of CCs or CSCs, providing an exciting, new area of knowledge to be investigated. This article reviews the progress to date in research on the role of inflammatory mediators and metabolic reprogramming during the carcinogenesis process of the thyroid gland and the EMT pathways.Universitat Autònoma de Barcelona 22019-01-0120192019-01-01Article de revisióhttp://purl.org/coar/resource_type/c_dcae04bcVoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://ddd.uab.cat/record/253288https://dx.doi.org/urn:doi:10.3390/ijms20102466reponame:Dipòsit Digital de Documents de la UABinstname:Universitat Autònoma de BarcelonaInglésengInstituto de Salud Carlos III https://doi.org/10.13039/501100004587 FIS16-00139open accesshttp://purl.org/coar/access_right/c_abf2Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.https://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:ddd.uab.cat:2532882026-06-06T12:50:31Z
dc.title.none.fl_str_mv Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid Carcinoma
title Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid Carcinoma
spellingShingle Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid Carcinoma
Revilla, Giovanna|||0000-0003-2971-5651
Thyroid carcinoma
Signaling pathways
MET/EMT
Leptin
Adiponectin
Low-density lipoproteins
High-density lipoproteins
title_short Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid Carcinoma
title_full Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid Carcinoma
title_fullStr Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid Carcinoma
title_full_unstemmed Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid Carcinoma
title_sort Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid Carcinoma
dc.creator.none.fl_str_mv Revilla, Giovanna|||0000-0003-2971-5651
Corcoy i Pla, Rosa|||0000-0001-5055-6814
Moral, Antonio|||0000-0001-5551-0145
Escolà-Gil, Joan Carles|||0000-0001-9021-2485
Mato, Eugènia|||0000-0001-8121-9335
author Revilla, Giovanna|||0000-0003-2971-5651
author_facet Revilla, Giovanna|||0000-0003-2971-5651
Corcoy i Pla, Rosa|||0000-0001-5055-6814
Moral, Antonio|||0000-0001-5551-0145
Escolà-Gil, Joan Carles|||0000-0001-9021-2485
Mato, Eugènia|||0000-0001-8121-9335
author_role author
author2 Corcoy i Pla, Rosa|||0000-0001-5055-6814
Moral, Antonio|||0000-0001-5551-0145
Escolà-Gil, Joan Carles|||0000-0001-9021-2485
Mato, Eugènia|||0000-0001-8121-9335
author2_role author
author
author
author
dc.contributor.none.fl_str_mv Universitat Autònoma de Barcelona
dc.subject.none.fl_str_mv Thyroid carcinoma
Signaling pathways
MET/EMT
Leptin
Adiponectin
Low-density lipoproteins
High-density lipoproteins
topic Thyroid carcinoma
Signaling pathways
MET/EMT
Leptin
Adiponectin
Low-density lipoproteins
High-density lipoproteins
description There is strong association between inflammatory processes and their main metabolic mediators, such as leptin, adiponectin secretion, and low/high-density lipoproteins, with the cancer risk and aggressive behavior of solid tumors. In this scenario, cancer cells (CCs) and cancer stem cells (CSCs) have important roles. These cellular populations, which come from differentiated cells and progenitor stem cells, have increased metabolic requirements when it comes to maintaining or expanding the tumors, and they serve as links to some inflammatory mediators. Although the molecular mechanisms that are involved in these associations remain unclear, the two following cellular pathways have been suggested: 1) the mesenchymal-epithelial transition (MET) process, which permits the differentiation of adult stem cells throughout the acquisition of cell polarity and the adhesion to epithelia, as well to new cellular lineages (CSCs); and, 2) a reverse process, termed the epithelial-mesenchymal transition (EMT), where, in pathophysiological conditions (tissue injury, inflammatory process, and oxidative stress), the differentiated cells can acquire a multipotent stem cell-like phenotype. The molecular mechanisms that regulate both EMT and MET are complex and poorly understood. Especially, in the thyroid gland, little is known regarding MET/EMT and the role of CCs or CSCs, providing an exciting, new area of knowledge to be investigated. This article reviews the progress to date in research on the role of inflammatory mediators and metabolic reprogramming during the carcinogenesis process of the thyroid gland and the EMT pathways.
publishDate 2019
dc.date.none.fl_str_mv 2
2019-01-01
2019
2019-01-01
dc.type.none.fl_str_mv Article de revisió
http://purl.org/coar/resource_type/c_dcae04bc
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://ddd.uab.cat/record/253288
https://dx.doi.org/urn:doi:10.3390/ijms20102466
url https://ddd.uab.cat/record/253288
https://dx.doi.org/urn:doi:10.3390/ijms20102466
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.relation.none.fl_str_mv Instituto de Salud Carlos III https://doi.org/10.13039/501100004587 FIS16-00139
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:Dipòsit Digital de Documents de la UAB
instname:Universitat Autònoma de Barcelona
instname_str Universitat Autònoma de Barcelona
reponame_str Dipòsit Digital de Documents de la UAB
collection Dipòsit Digital de Documents de la UAB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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