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Proteoglycans in the Pathogenesis of Hormone-Dependent Cancers: Mediators and Effectors

Hormone-dependent cancers exhibit high morbidity and mortality. In spite of advances in therapy, the treatment of hormone-dependent cancers remains an unmet health need. The tumor microenvironment (TME) exhibits unique characteristics that differ among various tumor types. It is composed of cancerou...

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Autores principales: Tzanakakis, George, Giatagana, Eirini-Maria, Kuskov, Andrey, Berdiaki, Aikaterini, Tsatsakis, Aristidis, Neagu, Monica, Nikitovic, Dragana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7563227/
https://www.ncbi.nlm.nih.gov/pubmed/32847060
http://dx.doi.org/10.3390/cancers12092401
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author Tzanakakis, George
Giatagana, Eirini-Maria
Kuskov, Andrey
Berdiaki, Aikaterini
Tsatsakis, Aristidis
Neagu, Monica
Nikitovic, Dragana
author_facet Tzanakakis, George
Giatagana, Eirini-Maria
Kuskov, Andrey
Berdiaki, Aikaterini
Tsatsakis, Aristidis
Neagu, Monica
Nikitovic, Dragana
author_sort Tzanakakis, George
collection PubMed
description Hormone-dependent cancers exhibit high morbidity and mortality. In spite of advances in therapy, the treatment of hormone-dependent cancers remains an unmet health need. The tumor microenvironment (TME) exhibits unique characteristics that differ among various tumor types. It is composed of cancerous, non-cancerous, stromal, and immune cells that are surrounded and supported by components of the extracellular matrix (ECM). Therefore, the interactions among cancer cells, stromal cells, and components of the ECM determine cancer progression and response to therapy. Proteoglycans (PGs), hybrid molecules consisting of a protein core to which sulfated glycosaminoglycan chains are bound, are significant components of the ECM that are implicated in all phases of tumorigenesis. These molecules, secreted by both the stroma and cancer cells, are crucial signaling mediators that modulate the vital cellular pathways implicated in gene expression, phenotypic versatility, and response to therapy in specific tumor types. A plethora of deregulated signaling pathways contributes to the growth, dissemination, and angiogenesis of hormone-dependent cancers. Specific inputs from the endocrine and immune systems are some of the characteristics of hormone-dependent cancer pathogenesis. Importantly, the mechanisms involved in various aspects of cancer progression are executed in the ECM niche of the TME, and the PG components crucially mediate these processes. Here, we comprehensively discuss the mechanisms through which PGs affect the multifaceted aspects of hormone-dependent cancer development and progression, including cancer metastasis, angiogenesis, immunobiology, autophagy, and response to therapy.
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spelling pubmed-75632272020-10-27 Proteoglycans in the Pathogenesis of Hormone-Dependent Cancers: Mediators and Effectors Tzanakakis, George Giatagana, Eirini-Maria Kuskov, Andrey Berdiaki, Aikaterini Tsatsakis, Aristidis Neagu, Monica Nikitovic, Dragana Cancers (Basel) Review Hormone-dependent cancers exhibit high morbidity and mortality. In spite of advances in therapy, the treatment of hormone-dependent cancers remains an unmet health need. The tumor microenvironment (TME) exhibits unique characteristics that differ among various tumor types. It is composed of cancerous, non-cancerous, stromal, and immune cells that are surrounded and supported by components of the extracellular matrix (ECM). Therefore, the interactions among cancer cells, stromal cells, and components of the ECM determine cancer progression and response to therapy. Proteoglycans (PGs), hybrid molecules consisting of a protein core to which sulfated glycosaminoglycan chains are bound, are significant components of the ECM that are implicated in all phases of tumorigenesis. These molecules, secreted by both the stroma and cancer cells, are crucial signaling mediators that modulate the vital cellular pathways implicated in gene expression, phenotypic versatility, and response to therapy in specific tumor types. A plethora of deregulated signaling pathways contributes to the growth, dissemination, and angiogenesis of hormone-dependent cancers. Specific inputs from the endocrine and immune systems are some of the characteristics of hormone-dependent cancer pathogenesis. Importantly, the mechanisms involved in various aspects of cancer progression are executed in the ECM niche of the TME, and the PG components crucially mediate these processes. Here, we comprehensively discuss the mechanisms through which PGs affect the multifaceted aspects of hormone-dependent cancer development and progression, including cancer metastasis, angiogenesis, immunobiology, autophagy, and response to therapy. MDPI 2020-08-24 /pmc/articles/PMC7563227/ /pubmed/32847060 http://dx.doi.org/10.3390/cancers12092401 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Tzanakakis, George
Giatagana, Eirini-Maria
Kuskov, Andrey
Berdiaki, Aikaterini
Tsatsakis, Aristidis
Neagu, Monica
Nikitovic, Dragana
Proteoglycans in the Pathogenesis of Hormone-Dependent Cancers: Mediators and Effectors
title Proteoglycans in the Pathogenesis of Hormone-Dependent Cancers: Mediators and Effectors
title_full Proteoglycans in the Pathogenesis of Hormone-Dependent Cancers: Mediators and Effectors
title_fullStr Proteoglycans in the Pathogenesis of Hormone-Dependent Cancers: Mediators and Effectors
title_full_unstemmed Proteoglycans in the Pathogenesis of Hormone-Dependent Cancers: Mediators and Effectors
title_short Proteoglycans in the Pathogenesis of Hormone-Dependent Cancers: Mediators and Effectors
title_sort proteoglycans in the pathogenesis of hormone-dependent cancers: mediators and effectors
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7563227/
https://www.ncbi.nlm.nih.gov/pubmed/32847060
http://dx.doi.org/10.3390/cancers12092401
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