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Cancer-Associated Adipocytes in Breast Cancer: Causes and Consequences

Breast cancer progression is highly dependent on the heterotypic interaction between tumor cells and stromal cells of the tumor microenvironment. Cancer-associated adipocytes (CAAs) are emerging as breast cancer cell partners favoring proliferation, invasion, and metastasis. This article discussed t...

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Detalles Bibliográficos
Autores principales: Rybinska, Ilona, Mangano, Nunzia, Tagliabue, Elda, Triulzi, Tiziana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8038661/
https://www.ncbi.nlm.nih.gov/pubmed/33917351
http://dx.doi.org/10.3390/ijms22073775
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author Rybinska, Ilona
Mangano, Nunzia
Tagliabue, Elda
Triulzi, Tiziana
author_facet Rybinska, Ilona
Mangano, Nunzia
Tagliabue, Elda
Triulzi, Tiziana
author_sort Rybinska, Ilona
collection PubMed
description Breast cancer progression is highly dependent on the heterotypic interaction between tumor cells and stromal cells of the tumor microenvironment. Cancer-associated adipocytes (CAAs) are emerging as breast cancer cell partners favoring proliferation, invasion, and metastasis. This article discussed the intersection between extracellular signals and the transcriptional cascade that regulates adipocyte differentiation in order to appreciate the molecular pathways that have been described to drive adipocyte dedifferentiation. Moreover, recent studies on the mechanisms through which CAAs affect the progression of breast cancer were reviewed, including adipokine regulation, metabolic reprogramming, extracellular matrix remodeling, and immune cell modulation. An in-depth understanding of the complex vicious cycle between CAAs and breast cancer cells is crucial for designing novel strategies for new therapeutic interventions.
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spelling pubmed-80386612021-04-12 Cancer-Associated Adipocytes in Breast Cancer: Causes and Consequences Rybinska, Ilona Mangano, Nunzia Tagliabue, Elda Triulzi, Tiziana Int J Mol Sci Review Breast cancer progression is highly dependent on the heterotypic interaction between tumor cells and stromal cells of the tumor microenvironment. Cancer-associated adipocytes (CAAs) are emerging as breast cancer cell partners favoring proliferation, invasion, and metastasis. This article discussed the intersection between extracellular signals and the transcriptional cascade that regulates adipocyte differentiation in order to appreciate the molecular pathways that have been described to drive adipocyte dedifferentiation. Moreover, recent studies on the mechanisms through which CAAs affect the progression of breast cancer were reviewed, including adipokine regulation, metabolic reprogramming, extracellular matrix remodeling, and immune cell modulation. An in-depth understanding of the complex vicious cycle between CAAs and breast cancer cells is crucial for designing novel strategies for new therapeutic interventions. MDPI 2021-04-06 /pmc/articles/PMC8038661/ /pubmed/33917351 http://dx.doi.org/10.3390/ijms22073775 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Rybinska, Ilona
Mangano, Nunzia
Tagliabue, Elda
Triulzi, Tiziana
Cancer-Associated Adipocytes in Breast Cancer: Causes and Consequences
title Cancer-Associated Adipocytes in Breast Cancer: Causes and Consequences
title_full Cancer-Associated Adipocytes in Breast Cancer: Causes and Consequences
title_fullStr Cancer-Associated Adipocytes in Breast Cancer: Causes and Consequences
title_full_unstemmed Cancer-Associated Adipocytes in Breast Cancer: Causes and Consequences
title_short Cancer-Associated Adipocytes in Breast Cancer: Causes and Consequences
title_sort cancer-associated adipocytes in breast cancer: causes and consequences
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8038661/
https://www.ncbi.nlm.nih.gov/pubmed/33917351
http://dx.doi.org/10.3390/ijms22073775
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