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High endogenous CCL2 expression promotes the aggressive phenotype of human inflammatory breast cancer
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High endogenous CCL2 expression promotes the aggressive phenotype of human inflammatory breast cancer
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Journal Article
High endogenous CCL2 expression promotes the aggressive phenotype of human inflammatory breast cancer
2021
Overview
Inflammatory Breast Cancer (IBC) is a highly aggressive malignancy with distinct clinical and histopathological features whose molecular basis is unresolved. Here we describe a human IBC cell line, A3250, that recapitulates key IBC features in a mouse xenograft model, including skin erythema, diffuse tumor growth, dermal lymphatic invasion, and extensive metastases. A3250 cells express very high levels of the CCL2 chemokine and induce tumors enriched in macrophages. CCL2 knockdown leads to a striking reduction in macrophage densities, tumor proliferation, skin erythema, and metastasis. These results establish IBC-derived CCL2 as a key factor driving macrophage expansion, and indirectly tumor growth, with transcriptomic analysis demonstrating the activation of multiple inflammatory pathways. Finally, primary human IBCs exhibit macrophage infiltration and an enriched macrophage RNA signature. Thus, this human IBC model provides insight into the distinctive biology of IBC, and highlights potential therapeutic approaches to this deadly disease.
Inflammatory breast cancer (IBC) is an aggressive form of breast cancer with a poor prognosis. Here the authors report the characterization of a human IBC cell line recapitulating the clinical and histopathological features of the human disease, and implicating its high level of CCL2 in macrophage infiltration and tumor progression.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/106
/ 13/109
/ 13/21
/ 13/44
/ 13/51
/ 14/1
/ 14/19
/ 14/5
/ 14/63
/ 38/61
/ 38/91
/ 59/5
/ 64/60
/ Animals
/ Erythema
/ Female
/ Gene Expression Regulation, Neoplastic
/ Humanities and Social Sciences
/ Humans
/ Inflammatory Breast Neoplasms
/ Inflammatory Breast Neoplasms - genetics
/ Inflammatory Breast Neoplasms - immunology
/ Inflammatory Breast Neoplasms - metabolism
/ Inflammatory Breast Neoplasms - pathology
/ Mice
/ Monocyte chemoattractant protein 1
/ Receptors, CCR2 - metabolism
/ Science
/ Transplantation, Heterologous
/ Tumor Microenvironment - immunology
/ Tumor-Associated Macrophages
/ Tumor-Associated Macrophages - immunology
/ Tumor-Associated Macrophages - pathology
/ Tumors
