Exploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy

The tumor microenvironment (TME) is composed of a heterogenous population of cells that exist alongside the extracellular matrix and soluble components. These components can shape an environment that is conducive to tumor growth and metastatic spread. It is well-established that stromal cancer-assoc...

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Autores principales: Amr Allam, Marina Yakou, Lokman Pang, Matthias Ernst, Jennifer Huynh
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Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/d4a5077b598e480abc59c2ccf7573b8a
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spelling oai:doaj.org-article:d4a5077b598e480abc59c2ccf7573b8a2021-11-11T08:33:05ZExploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy1664-322410.3389/fimmu.2021.767939https://doaj.org/article/d4a5077b598e480abc59c2ccf7573b8a2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.767939/fullhttps://doaj.org/toc/1664-3224The tumor microenvironment (TME) is composed of a heterogenous population of cells that exist alongside the extracellular matrix and soluble components. These components can shape an environment that is conducive to tumor growth and metastatic spread. It is well-established that stromal cancer-associated fibroblasts (CAFs) in the TME play a pivotal role in creating and maintaining a growth-permissive environment for tumor cells. A growing body of work has uncovered that tumor cells recruit and educate CAFs to remodel the TME, however, the mechanisms by which this occurs remain incompletely understood. Recent studies suggest that the signal transducer and activator of transcription 3 (STAT3) is a key transcription factor that regulates the function of CAFs, and their crosstalk with tumor and immune cells within the TME. CAF-intrinsic STAT3 activity within the TME correlates with tumor progression, immune suppression and eventually the establishment of metastases. In this review, we will focus on the roles of STAT3 in regulating CAF function and their crosstalk with other cells constituting the TME and discuss the utility of targeting STAT3 within the TME for therapeutic benefit.Amr AllamMarina YakouLokman PangMatthias ErnstJennifer HuynhFrontiers Media S.A.articleSTAT (signal transducer and activator of transcription)tumor developmentcancer associated fibroblasts (CAF)cytokinestumor microenvironmentImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic STAT (signal transducer and activator of transcription)
tumor development
cancer associated fibroblasts (CAF)
cytokines
tumor microenvironment
Immunologic diseases. Allergy
RC581-607
spellingShingle STAT (signal transducer and activator of transcription)
tumor development
cancer associated fibroblasts (CAF)
cytokines
tumor microenvironment
Immunologic diseases. Allergy
RC581-607
Amr Allam
Marina Yakou
Lokman Pang
Matthias Ernst
Jennifer Huynh
Exploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy
description The tumor microenvironment (TME) is composed of a heterogenous population of cells that exist alongside the extracellular matrix and soluble components. These components can shape an environment that is conducive to tumor growth and metastatic spread. It is well-established that stromal cancer-associated fibroblasts (CAFs) in the TME play a pivotal role in creating and maintaining a growth-permissive environment for tumor cells. A growing body of work has uncovered that tumor cells recruit and educate CAFs to remodel the TME, however, the mechanisms by which this occurs remain incompletely understood. Recent studies suggest that the signal transducer and activator of transcription 3 (STAT3) is a key transcription factor that regulates the function of CAFs, and their crosstalk with tumor and immune cells within the TME. CAF-intrinsic STAT3 activity within the TME correlates with tumor progression, immune suppression and eventually the establishment of metastases. In this review, we will focus on the roles of STAT3 in regulating CAF function and their crosstalk with other cells constituting the TME and discuss the utility of targeting STAT3 within the TME for therapeutic benefit.
format article
author Amr Allam
Marina Yakou
Lokman Pang
Matthias Ernst
Jennifer Huynh
author_facet Amr Allam
Marina Yakou
Lokman Pang
Matthias Ernst
Jennifer Huynh
author_sort Amr Allam
title Exploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy
title_short Exploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy
title_full Exploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy
title_fullStr Exploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy
title_full_unstemmed Exploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy
title_sort exploiting the stat3 nexus in cancer-associated fibroblasts to improve cancer therapy
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/d4a5077b598e480abc59c2ccf7573b8a
work_keys_str_mv AT amrallam exploitingthestat3nexusincancerassociatedfibroblaststoimprovecancertherapy
AT marinayakou exploitingthestat3nexusincancerassociatedfibroblaststoimprovecancertherapy
AT lokmanpang exploitingthestat3nexusincancerassociatedfibroblaststoimprovecancertherapy
AT matthiasernst exploitingthestat3nexusincancerassociatedfibroblaststoimprovecancertherapy
AT jenniferhuynh exploitingthestat3nexusincancerassociatedfibroblaststoimprovecancertherapy
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