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巨噬细胞炎症因子促进乳腺癌上皮-间质转化。

Macrophage inflammatory factors promote epithelial-mesenchymal transition in breast cancer.

作者信息

Bednarczyk Robert B, Tuli Neha Y, Hanly Elyse K, Rahoma Ghada Ben, Maniyar Rachana, Mittelman Abraham, Geliebter Jan, Tiwari Raj K

机构信息

Department of Microbiology and Immunology, New York Medical College, Valhalla, NY, USA.

出版信息

Oncotarget. 2018 Mar 23;9(36):24272-24282. doi: 10.18632/oncotarget.24917. eCollection 2018 May 11.

DOI:10.18632/oncotarget.24917
PMID:29849939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5966261/
Abstract

The majority of breast cancers (90-95%) arise due to mediators distinct from inherited genetic mutations. One major mediator of breast cancer involves chronic inflammation. M1 macrophages are an integral component of chronic inflammation and the breast cancer tumor microenvironment (TME). Previous studies have demonstrated that up to 50% of the breast tumor comprise of tumor-associated macrophages (TAMs) and increased TAM infiltration has been associated with poor patient prognosis. Furthermore, breast cancer associated deaths are predominantly attributed to invasive cancers and metastasis with epithelial-mesenchymal transition (EMT) being implicated. In this study, we investigated the effects of cellular crosstalk between TAMs and breast cancer using an model system. M1 polarized THP-1 macrophage conditioned media (CM) was generated and used to evaluate cellular and functional changes of breast cancer lines T47D and MCF-7. We observed that T47D and MCF-7 exhibited a partial EMT phenotype in the presence of activated THP-1 CM. Additionally, MCF-7 displayed a significant increase in migratory and invasive properties. We conclude that M1 secretory factors can promote a partial EMT of epithelial-like breast cancer cells. The targeting of M1 macrophages or their secretory components may inhibit EMT and limit the invasive potential of breast cancer.

摘要

大多数乳腺癌（90-95%）是由与遗传性基因突变不同的介质引起的。乳腺癌的一个主要介质涉及慢性炎症。M1巨噬细胞是慢性炎症和乳腺癌肿瘤微环境（TME）的一个组成部分。先前的研究表明，高达50%的乳腺肿瘤由肿瘤相关巨噬细胞（TAM）组成，TAM浸润增加与患者预后不良有关。此外，乳腺癌相关死亡主要归因于侵袭性癌症和转移，其中上皮-间质转化（EMT）也有涉及。在本研究中，我们使用一种模型系统研究了TAM与乳腺癌之间的细胞间相互作用的影响。生成了M1极化的THP-1巨噬细胞条件培养基（CM），并用于评估乳腺癌细胞系T47D和MCF-7的细胞和功能变化。我们观察到，在活化的THP-1 CM存在下，T47D和MCF-7表现出部分EMT表型。此外，MCF-7的迁移和侵袭特性显著增加。我们得出结论，M1分泌因子可促进上皮样乳腺癌细胞的部分EMT。靶向M1巨噬细胞或其分泌成分可能抑制EMT并限制乳腺癌的侵袭潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/0894d90ac881/oncotarget-09-24272-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/631ee66a33f6/oncotarget-09-24272-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/96ce01e88646/oncotarget-09-24272-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/1083e6a2e149/oncotarget-09-24272-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/850b5d6a5c42/oncotarget-09-24272-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/35669dfe9fbc/oncotarget-09-24272-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/0894d90ac881/oncotarget-09-24272-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/631ee66a33f6/oncotarget-09-24272-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/96ce01e88646/oncotarget-09-24272-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/1083e6a2e149/oncotarget-09-24272-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/850b5d6a5c42/oncotarget-09-24272-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/35669dfe9fbc/oncotarget-09-24272-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8272/5966261/0894d90ac881/oncotarget-09-24272-g006.jpg

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