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“UPRegulation” of CD47 by the endoplasmic reticulum stress pathway controls anti-tumor immune responses

We recently demonstrated that targeting the unfolded protein response (UPR) protein GRP78 down-regulates CD47 expression, resulting in increased tumor macrophage infiltration and inhibited resistance to anti-estrogen therapy. We now show new data indicating that anti-estrogen therapy regulates CD47...

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Detalles Bibliográficos
Autores principales: Cook, Katherine L., Soto-Pantoja, David R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5557514/
https://www.ncbi.nlm.nih.gov/pubmed/28815041
http://dx.doi.org/10.1186/s40364-017-0105-8
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author Cook, Katherine L.
Soto-Pantoja, David R.
author_facet Cook, Katherine L.
Soto-Pantoja, David R.
author_sort Cook, Katherine L.
collection PubMed
description We recently demonstrated that targeting the unfolded protein response (UPR) protein GRP78 down-regulates CD47 expression, resulting in increased tumor macrophage infiltration and inhibited resistance to anti-estrogen therapy. We now show new data indicating that anti-estrogen therapy regulates CD47 expression and implicates its ligand, thrombospondin-1, in regulation of tumor macrophage infiltration. Moreover, GRP78 and CD47 co-expression is associated with poor prognosis in breast cancer patients, suggesting the existence of crosstalk between UPR and immunity that regulates therapeutic responses in breast cancer.
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spelling pubmed-55575142017-08-16 “UPRegulation” of CD47 by the endoplasmic reticulum stress pathway controls anti-tumor immune responses Cook, Katherine L. Soto-Pantoja, David R. Biomark Res Short Report We recently demonstrated that targeting the unfolded protein response (UPR) protein GRP78 down-regulates CD47 expression, resulting in increased tumor macrophage infiltration and inhibited resistance to anti-estrogen therapy. We now show new data indicating that anti-estrogen therapy regulates CD47 expression and implicates its ligand, thrombospondin-1, in regulation of tumor macrophage infiltration. Moreover, GRP78 and CD47 co-expression is associated with poor prognosis in breast cancer patients, suggesting the existence of crosstalk between UPR and immunity that regulates therapeutic responses in breast cancer. BioMed Central 2017-08-14 /pmc/articles/PMC5557514/ /pubmed/28815041 http://dx.doi.org/10.1186/s40364-017-0105-8 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Short Report
Cook, Katherine L.
Soto-Pantoja, David R.
“UPRegulation” of CD47 by the endoplasmic reticulum stress pathway controls anti-tumor immune responses
title “UPRegulation” of CD47 by the endoplasmic reticulum stress pathway controls anti-tumor immune responses
title_full “UPRegulation” of CD47 by the endoplasmic reticulum stress pathway controls anti-tumor immune responses
title_fullStr “UPRegulation” of CD47 by the endoplasmic reticulum stress pathway controls anti-tumor immune responses
title_full_unstemmed “UPRegulation” of CD47 by the endoplasmic reticulum stress pathway controls anti-tumor immune responses
title_short “UPRegulation” of CD47 by the endoplasmic reticulum stress pathway controls anti-tumor immune responses
title_sort “upregulation” of cd47 by the endoplasmic reticulum stress pathway controls anti-tumor immune responses
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5557514/
https://www.ncbi.nlm.nih.gov/pubmed/28815041
http://dx.doi.org/10.1186/s40364-017-0105-8
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