MicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancer

Abstract Many immune suppressive mechanisms utilized by triple negative breast cancer (TNBC) are regulated by oncogenic epithelial-to-mesenchymal transition (EMT). How TNBC EMT impacts innate immune cells is not fully understood. To determine how TNBC suppresses antitumor macrophages, we used microR...

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Autores principales:	Michelle M. Williams, Jessica L. Christenson, Kathleen I. O’Neill, Sabrina A. Hafeez, Claire L. Ihle, Nicole S. Spoelstra, Jill E. Slansky, Jennifer K. Richer
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/60e89acc1885465fafd6cd0d4bea2bf5
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spelling	oai:doaj.org-article:60e89acc1885465fafd6cd0d4bea2bf52021-12-02T15:49:26ZMicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancer10.1038/s41523-021-00273-12374-4677https://doaj.org/article/60e89acc1885465fafd6cd0d4bea2bf52021-05-01T00:00:00Zhttps://doi.org/10.1038/s41523-021-00273-1https://doaj.org/toc/2374-4677Abstract Many immune suppressive mechanisms utilized by triple negative breast cancer (TNBC) are regulated by oncogenic epithelial-to-mesenchymal transition (EMT). How TNBC EMT impacts innate immune cells is not fully understood. To determine how TNBC suppresses antitumor macrophages, we used microRNA-200c (miR-200c), a powerful repressor of EMT, to drive mesenchymal-like mouse mammary carcinoma and human TNBC cells toward a more epithelial state. MiR-200c restoration significantly decreased growth of mouse mammary carcinoma Met-1 cells in culture and in vivo. Cytokine profiling of Met-1 and human BT549 cells revealed that miR-200c upregulated cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), promoted M1 antitumor macrophage polarization. Cytokines upregulated by miR-200c correlated with an epithelial gene signature and M1 macrophage polarization in BC patients and predicted a more favorable overall survival for TNBC patients. Our findings demonstrate that immunogenic cytokines (e.g., GM-CSF) are suppressed in aggressive TNBC, warranting further investigation of cytokine-based therapies to limit disease recurrence.Michelle M. WilliamsJessica L. ChristensonKathleen I. O’NeillSabrina A. HafeezClaire L. IhleNicole S. SpoelstraJill E. SlanskyJennifer K. RicherNature PortfolioarticleNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENnpj Breast Cancer, Vol 7, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Michelle M. Williams Jessica L. Christenson Kathleen I. O’Neill Sabrina A. Hafeez Claire L. Ihle Nicole S. Spoelstra Jill E. Slansky Jennifer K. Richer MicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancer
description	Abstract Many immune suppressive mechanisms utilized by triple negative breast cancer (TNBC) are regulated by oncogenic epithelial-to-mesenchymal transition (EMT). How TNBC EMT impacts innate immune cells is not fully understood. To determine how TNBC suppresses antitumor macrophages, we used microRNA-200c (miR-200c), a powerful repressor of EMT, to drive mesenchymal-like mouse mammary carcinoma and human TNBC cells toward a more epithelial state. MiR-200c restoration significantly decreased growth of mouse mammary carcinoma Met-1 cells in culture and in vivo. Cytokine profiling of Met-1 and human BT549 cells revealed that miR-200c upregulated cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), promoted M1 antitumor macrophage polarization. Cytokines upregulated by miR-200c correlated with an epithelial gene signature and M1 macrophage polarization in BC patients and predicted a more favorable overall survival for TNBC patients. Our findings demonstrate that immunogenic cytokines (e.g., GM-CSF) are suppressed in aggressive TNBC, warranting further investigation of cytokine-based therapies to limit disease recurrence.
format	article
author	Michelle M. Williams Jessica L. Christenson Kathleen I. O’Neill Sabrina A. Hafeez Claire L. Ihle Nicole S. Spoelstra Jill E. Slansky Jennifer K. Richer
author_facet	Michelle M. Williams Jessica L. Christenson Kathleen I. O’Neill Sabrina A. Hafeez Claire L. Ihle Nicole S. Spoelstra Jill E. Slansky Jennifer K. Richer
author_sort	Michelle M. Williams
title	MicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancer
title_short	MicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancer
title_full	MicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancer
title_fullStr	MicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancer
title_full_unstemmed	MicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancer
title_sort	microrna-200c restoration reveals a cytokine profile to enhance m1 macrophage polarization in breast cancer
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/60e89acc1885465fafd6cd0d4bea2bf5
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MicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancer

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