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Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma

Transforming growth factor-β (TGF-β) is a pleiotropic growth factor with broad tissue distribution that plays critical roles during embryonic development, normal tissue homeostasis, and cancer. While its cytostatic activity on normal epithelial cells initially defined TGF-β signaling as a tumor supp...

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Autores principales: Perrot, Carole Yolande, Javelaud, Delphine, Mauviel, Alain
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Dermatological Association; The Korean Society for Investigative Dermatology 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3662904/
https://www.ncbi.nlm.nih.gov/pubmed/23717002
http://dx.doi.org/10.5021/ad.2013.25.2.135
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author Perrot, Carole Yolande
Javelaud, Delphine
Mauviel, Alain
author_facet Perrot, Carole Yolande
Javelaud, Delphine
Mauviel, Alain
author_sort Perrot, Carole Yolande
collection PubMed
description Transforming growth factor-β (TGF-β) is a pleiotropic growth factor with broad tissue distribution that plays critical roles during embryonic development, normal tissue homeostasis, and cancer. While its cytostatic activity on normal epithelial cells initially defined TGF-β signaling as a tumor suppressor pathway, there is ample evidence indicating that TGF-β is a potent pro-tumorigenic agent, acting via autocrine and paracrine mechanisms to promote peri-tumoral angiogenesis, together with tumor cell migration, immune escape, and dissemination to metastatic sites. This review summarizes the current knowledge on the implication of TGF-β signaling in melanoma.
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spelling pubmed-36629042013-05-28 Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma Perrot, Carole Yolande Javelaud, Delphine Mauviel, Alain Ann Dermatol Review Article Transforming growth factor-β (TGF-β) is a pleiotropic growth factor with broad tissue distribution that plays critical roles during embryonic development, normal tissue homeostasis, and cancer. While its cytostatic activity on normal epithelial cells initially defined TGF-β signaling as a tumor suppressor pathway, there is ample evidence indicating that TGF-β is a potent pro-tumorigenic agent, acting via autocrine and paracrine mechanisms to promote peri-tumoral angiogenesis, together with tumor cell migration, immune escape, and dissemination to metastatic sites. This review summarizes the current knowledge on the implication of TGF-β signaling in melanoma. Korean Dermatological Association; The Korean Society for Investigative Dermatology 2013-05 2013-05-10 /pmc/articles/PMC3662904/ /pubmed/23717002 http://dx.doi.org/10.5021/ad.2013.25.2.135 Text en Copyright © 2013 The Korean Dermatological Association and The Korean Society for Investigative Dermatology http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Perrot, Carole Yolande
Javelaud, Delphine
Mauviel, Alain
Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma
title Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma
title_full Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma
title_fullStr Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma
title_full_unstemmed Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma
title_short Insights into the Transforming Growth Factor-β Signaling Pathway in Cutaneous Melanoma
title_sort insights into the transforming growth factor-β signaling pathway in cutaneous melanoma
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3662904/
https://www.ncbi.nlm.nih.gov/pubmed/23717002
http://dx.doi.org/10.5021/ad.2013.25.2.135
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