Characterization of macrophage - cancer cell crosstalk in estrogen receptor positive and triple-negative breast cancer


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Date

2015-03-17

Publication Type

Journal Article

ETH Bibliography

yes

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Data

Abstract

Tumor heterogeneity may broadly influence the activation of tumor-associated macrophages. We aimed to dissect how breast cancer cells of different molecular characteristics contribute to macrophage phenotype and function. Therefore, we performed whole transcriptome sequencing of human monocytes that were co-cultured with estrogen receptor positive (ER+) or triple-negative (TNBC) breast cancer cell lines and studied the biological responses related to the differential gene activation in both monocytes and cancer cells by pathway analysis. ER+ and TNBC cancer cell lines induced distinctly different macrophage phenotypes with different biological functions, cytokine and chemokine secretion, and morphology. Conversely, ER+ and TNBC breast cancer cell lines were distinctly influenced by the presence of macrophages. ER+ cells demonstrated up-regulation of an acute phase inflammatory response, IL-17 signaling and antigen presentation pathway, whereas thioredoxin and vitamin D3 receptor pathways were down-regulated in the respective macrophages. The TNBC educated macrophages down-regulated citrulline metabolism and differentiated into M2-like macrophages with increased MMR protein expression and CCL2 secretion. These data demonstrate how different cancer cells educate the host cells to support tumor growth and might explain why high infiltration of macrophages in TNBC tumors associates with poor prognosis.

Publication status

published

Editor

Book title

Volume

5

Pages / Article No.

9188

Publisher

Nature

Event

Edition / version

Methods

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Geographic location

Date collected

Date created

Subject

Breast cancer; Gene regulation in immune cells

Organisational unit

03683 - Detmar, Michael (emeritus) / Detmar, Michael (emeritus) check_circle

Notes

Funding

147087 - Molecular mechanisms of angiogenesis and lymphangiogenesis in inflammation and cancer progression (SNF)

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