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Macrophages of M1 phenotype have properties that influence lung cancer cell progression
Department of Health Sciences, Karlstad University, Karlstad, Sweden.
Department of Health Sciences, Karlstad University, Karlstad, Sweden.
Department of Health Sciences, Karlstad University, Karlstad, Sweden.
Örebro universitet, Institutionen för läkarutbildning.
Vise andre og tillknytning
2015 (engelsk)Inngår i: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 36, nr 11, s. 8715-8725Artikkel i tidsskrift (Fagfellevurdert) Published
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Abstract [en]

Stromal macrophages of different phenotypes can contribute to the expression of proteins that affects metastasis such as urokinase-type plasminogen activator (uPA), its receptor uPAR, and plasminogen activator inhibitor-1 (PAI-1), but knowledge of how essential their contribution is in comparison to the cancer cells in small cell lung cancer (SCLC) and lung squamous cell carcinoma (SCC) is lacking. The expression of uPA, uPAR, and PAI-1 and of the matrix metalloproteinases (MMP)-2 and MMP-9 were studied in human macrophages of M1 and M2 phenotype and compared to a lung SCC (NCI-H520) and a SCLC (NCI-H69) cell line. Effects of treatment with conditioned media (CM) from M1 and M2 macrophages on the expression of these genes in H520 and H69 cells as well as effects on the cell growth were investigated. In addition, data on the stromal macrophages immunoreactivity of uPAR, MMP-2, and MMP-9 in a few SCC and SCLC biopsies was included. uPAR, MMP-2, and MMP-9 were confirmed in stromal cells including macrophages in the SCC and SCLC biopsies. In vitro, both macrophage phenotypes expressed considerably higher mRNA levels of uPA, uPAR, PAI-1, and MMP-9 compared to the cancer cell lines, and regarding uPAR, the highest level was found in the M1 macrophage phenotype. Furthermore, M1 CM treatment not only induced an upregulation of PAI-1 in both H520 and H69 cells but also inhibited cell growth in both cell lines, giving M1 macrophages both tumor-promoting and tumor-killing potential.

sted, utgiver, år, opplag, sider
Springer, 2015. Vol. 36, nr 11, s. 8715-8725
Emneord [en]
M1 macrophages, M2 macrophages, MMP, Lung cancer, uPA, uPAR
HSV kategori
Forskningsprogram
Onkologi
Identifikatorer
URN: urn:nbn:se:oru:diva-47303DOI: 10.1007/s13277-015-3630-9ISI: 000366143100059PubMedID: 26050228Scopus ID: 2-s2.0-84949099755OAI: oai:DiVA.org:oru-47303DiVA, id: diva2:890856
Merknad

Funding Agencies:

County Council of Värmland

Örebro University

Tilgjengelig fra: 2016-01-05 Laget: 2016-01-04 Sist oppdatert: 2017-12-01bibliografisk kontrollert

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