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Article: Melanoma-derived conditioned media efficiently induce the differentiation of monocytes to macrophages that display a highly invasive gene signature

TitleMelanoma-derived conditioned media efficiently induce the differentiation of monocytes to macrophages that display a highly invasive gene signature
Authors
KeywordsGlycoprotein non-metastatic melanoma protein B
Invasion
Macrophages
Melanoma
Tumor microenvironment
Issue Date2012
Citation
Pigment Cell and Melanoma Research, 2012, v. 25, n. 4, p. 493-505 How to Cite?
AbstractThe presence of tumor-associated macrophages (TAMs) in melanomas is correlated with a poor clinical prognosis. However, there is limited information on the characteristics and biological activities of human TAMs in melanomas. In this study, we developed an in vitro method to differentiate human monocytes to macrophages using modified melanoma-conditioned medium (MCM). We demonstrate that factors from MCM-induced macrophages (MCMI-Mφ) express both M1-Mφ and M2-Mφ markers and inhibit melanoma-specific T-cell proliferation. Furthermore, microarray analyses reveal that the majority of genes up-regulated in MCMI-Mφ are associated with tumor invasion. The most strikingly up-regulated genes are CCL2 and MMP-9. Consistent with this, blockade of both CCL-2 and MMPs diminish MCMI-Mφ-induced melanoma invasion. Finally, we demonstrated that both MCMI-Mφ and in vivo TAMs express the pro-invasive, melanoma-associated gene, glycoprotein non-metastatic melanoma protein B. Our study provides a framework for understanding the mechanisms of cross-talk between TAMs and melanoma cells within the tumor microenvironment. © 2012 John Wiley & Sons A/S.
Persistent Identifierhttp://hdl.handle.net/10722/318512
ISSN
2023 Impact Factor: 3.9
2023 SCImago Journal Rankings: 1.448
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, Tao-
dc.contributor.authorGe, Yingbin-
dc.contributor.authorXiao, Min-
dc.contributor.authorLopez-Coral, Alfonso-
dc.contributor.authorAzuma, Rikka-
dc.contributor.authorSomasundaram, Rajasekharan-
dc.contributor.authorZhang, Gao-
dc.contributor.authorWei, Zhi-
dc.contributor.authorXu, Xiaowei-
dc.contributor.authorRauscher, Frank J.-
dc.contributor.authorHerlyn, Meenhard-
dc.contributor.authorKaufman, Russel E.-
dc.date.accessioned2022-10-11T12:23:56Z-
dc.date.available2022-10-11T12:23:56Z-
dc.date.issued2012-
dc.identifier.citationPigment Cell and Melanoma Research, 2012, v. 25, n. 4, p. 493-505-
dc.identifier.issn1755-1471-
dc.identifier.urihttp://hdl.handle.net/10722/318512-
dc.description.abstractThe presence of tumor-associated macrophages (TAMs) in melanomas is correlated with a poor clinical prognosis. However, there is limited information on the characteristics and biological activities of human TAMs in melanomas. In this study, we developed an in vitro method to differentiate human monocytes to macrophages using modified melanoma-conditioned medium (MCM). We demonstrate that factors from MCM-induced macrophages (MCMI-Mφ) express both M1-Mφ and M2-Mφ markers and inhibit melanoma-specific T-cell proliferation. Furthermore, microarray analyses reveal that the majority of genes up-regulated in MCMI-Mφ are associated with tumor invasion. The most strikingly up-regulated genes are CCL2 and MMP-9. Consistent with this, blockade of both CCL-2 and MMPs diminish MCMI-Mφ-induced melanoma invasion. Finally, we demonstrated that both MCMI-Mφ and in vivo TAMs express the pro-invasive, melanoma-associated gene, glycoprotein non-metastatic melanoma protein B. Our study provides a framework for understanding the mechanisms of cross-talk between TAMs and melanoma cells within the tumor microenvironment. © 2012 John Wiley & Sons A/S.-
dc.languageeng-
dc.relation.ispartofPigment Cell and Melanoma Research-
dc.subjectGlycoprotein non-metastatic melanoma protein B-
dc.subjectInvasion-
dc.subjectMacrophages-
dc.subjectMelanoma-
dc.subjectTumor microenvironment-
dc.titleMelanoma-derived conditioned media efficiently induce the differentiation of monocytes to macrophages that display a highly invasive gene signature-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1755-148X.2012.01005.x-
dc.identifier.pmid22498258-
dc.identifier.scopuseid_2-s2.0-84862663385-
dc.identifier.volume25-
dc.identifier.issue4-
dc.identifier.spage493-
dc.identifier.epage505-
dc.identifier.eissn1755-148X-
dc.identifier.isiWOS:000305511200014-

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