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Effect of macrophages on breast cancer cell proliferation, and on expression of hormone receptors, uPAR and HER-2
Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden.
Örebro University, School of Medical Sciences.
Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden; School of Medical Sciences, Örebro University, Örebro, Sweden.
Department of Health Sciences, Karlstad University, Karlstad, Sweden.
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2017 (English)In: International Journal of Oncology, ISSN 1019-6439, Vol. 51, no 1, 104-114 p.Article in journal (Refereed) Published
Abstract [en]

Malignant tumors, including breast cancers, are frequently infiltrated with innate immune cells and tumor-associated macrophages (TAMs) represent the major inflammatory component in stroma of many tumors. In this study, we examined the immunoreactivity of the macrophage markers CD68 and CD163 as well as the hormone receptors estrogen receptor alpha (ER alpha), progesterone receptor (PR), estrogen receptor beta 1 (ER beta 1), human epidermal growth factor receptor 2 (HER-2), matrix metalloproteinase 9 (MMP-9), urokinase-type plasminogen activator receptor (uPAR) and the proliferations marker Ki67 in 17 breast cancer biopsies. The quantitative score for CD68(+) and CD163(+) strongly indicate M2 phenotype dominance in the currently investigated biopsies. We found that an increasing level of macrophages was negatively associated with ER alpha or PR, whereas a positive association was observed for Ki-67 or uPAR. No significant association could be seen between the level of macrophage and HER-2, ER beta 1 or MMP-9 expression. Effect of conditioned media (CM) generated from cultured human M1 and M2 macrophage phenotypes were investigated on the proliferation and expression of selected markers in the T47D breast cancer cell line. We found that in contrast to the in vivo situation, in particularly the CM from M1 macrophages decreased the growth and Ki67 expression in T47D, and significantly increased ER beta 1 mRNA levels. Moreover, in accordance to the in vivo situation the CM from the macrophages decreased the expression of ER alpha protein as well as ER alpha or PR mRNA. In conclusion our results show that macrophages alone have the capability to decrease the tumor cell expression of ER alpha and PR in vitro. In the tumor environment in vivo macrophages also contribute to an increase in tumor cell expression of uPAR and Ki67, suggesting that macrophages are involved in impairing the prognosis for breast cancer patients.

Place, publisher, year, edition, pages
Spandidos Publications , 2017. Vol. 51, no 1, 104-114 p.
Keyword [en]
breast cancer, breast cancer cell line, T47D, estrogen receptors, progesterone receptor, M1 macrophages, M2 macrophages, urokinase-type plasminogen activator receptor
National Category
Cancer and Oncology
Identifiers
URN: urn:nbn:se:oru:diva-58940DOI: 10.3892/ijo.2017.3996ISI: 000403994300009PubMedID: 28498427Scopus ID: 2-s2.0-85020544220OAI: oai:DiVA.org:oru-58940DiVA: diva2:1134389
Note

Funding Agencies:

County Council of Värmland  

Karlstad University  

Örebro University 

Available from: 2017-08-18 Created: 2017-08-18 Last updated: 2017-09-26Bibliographically approved

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Hedbrant, AlexanderDelbro, DickErlandsson, Ann
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