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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Oral squamous carcinoma cells promote macrophage polarization in an MIF-dependent manner

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Author(s):
de Souza Rizzo, M. Barbosa [1, 2, 3] ; Brasilino de Carvalho, M. [1, 2] ; Kim, E. J. [3] ; Rendon, B. E. [3] ; Noe, J. T. [3, 4] ; Wise, A. Darlene [3, 5] ; Mitchell, R. A. [3, 4, 5, 6]
Total Authors: 7
Affiliation:
[1] Univ Sao Paulo, Med Sch, Dept Radiol & Oncol, Sao Paulo, SP - Brazil
[2] Heliopolis Hosp, Lab Mol Biol, Sao Paulo, SP - Brazil
[3] Univ Louisville, JG Brown Canc Ctr, Louisville, KY 40292 - USA
[4] Univ Louisville, Dept Biochem & Mol Genet, Louisville, KY 40292 - USA
[5] Univ Louisville, Dept Microbiol & Immunol, Louisville, KY - USA
[6] Univ Louisville, Dept Med, Louisville, KY 40292 - USA
Total Affiliations: 6
Document type: Journal article
Source: QJM-AN INTERNATIONAL JOURNAL OF MEDICINE; v. 111, n. 11, p. 769-778, NOV 2018.
Web of Science Citations: 0
Abstract

Background: Tumor-associated macrophages (TAMs) are important determinants of intratumoral immune evasion, neoan-giogenesis, extracellular matrix remodeling and dysregulated tumor cell proliferation. Our prior studies revealed that macrophage-derived, but not tumor cell-derived, macrophage migration inhibitory factor (MIF), is an important determinant of TAM alternative activation and M2 polarization. Aim: Because MIF is historically thought to initiate signaling via a receptor-dependent, outside-in mode of action, we wished to investigate the specific contributions of tumor-derived vs. macrophage-derived MIF to M2 marker expression during macrophage polarization. Design: Murine oral squamous cell-carcinoma cells (SCCVII) were co-cultured with either the RAW 264.7 mouse macrophage cell line or mouse primary bone marrow-derived macrophages in the context of MIF genetic loss/inhibition individually or in combination each cell type. Methods: Twelve well Transwell plates were used to co-culture SCCVII cells and RAW 264.7, MIF+/+ or MIF-/- macrophages treated with/without the small molecule MIF inhibitor, 4-iodo-6-phenylpyrimidine and incubated in the presence or absence of interleukin (IL-4) for 48 h. Macrophages were analyzed by quantitative real-time polymerase chain reaction and/or immunoblotting for relative macrophage polarization marker expression. Results: IL-4 treatment synergizes with SCCVII co-culture in inducing the expression of macrophage M2 markers and loss or inhibition of macrophage-derived MIF significantly reduces both IL-4 alone and IL-4/SCCVII co-culture-induced macrophage M2 marker expression. Conclusion: These studies identify an important and dominant requirement for macrophage MIF in maximal Th2-cytokine and oral squamous carcinoma cell-induced macrophage polarization and M2 marker expression. (AU)

FAPESP's process: 15/15170-4 - Study of the role of the Macrophage Migration Inhibitory Factor in the modulation of the tumor inflammatory infiltrate and progression of oral squamous cell carcinoma
Grantee:Mariana Barbosa de Souza Rizzo
Support type: Scholarships abroad - Research Internship - Doctorate
FAPESP's process: 15/02584-5 - The role of the Macrophage Migration Inhibitory Factor in the modulation of the tumor inflammatory infiltrate and progression of oral squamous cell carcinoma
Grantee:Mariana Barbosa de Souza Rizzo
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 15/03453-1 - The role of cancer-associated inflammation in the regional dissemination of the oral squamous cell carcinoma
Grantee:Marcos Brasilino de Carvalho
Support type: Regular Research Grants