PT  - JOURNAL ARTICLE
AU  - GISELLE T. BURNETT
AU  - DENISE C. WEATHERSBY
AU  - TIFFANY E. TAYLOR
AU  - THEODORE A. BREMNER
TI  - Regulation of Inflammation- and Angiogenesis-related Gene Expression in Breast Cancer Cells and Co-cultured Macrophages
DP  - 2008 Jul 01
TA  - Anticancer Research
PG  - 2093--2099
VI  - 28
IP  - 4B
4099  - http://ar.iiarjournals.org/content/28/4B/2093.short
4100  - http://ar.iiarjournals.org/content/28/4B/2093.full
SO  - Anticancer Res2008 Jul 01; 28
AB  - Background: Tumor-associated macrophages (TAMs) secrete key modifiers of tumor progression and their modification has been proposed as a therapeutic strategy. Phenotypic changes that may render TAMs selectively vulnerable to anti-cancer agents were examined. Materials and Methods: Gene arrays, reverse transcription-polymerase chain reaction and Western blotting were used to study inflammation- and angiogenesis-related gene expression in co-cultured breast cancer cells and macrophages and to determine how their interactions were affected by tamoxifen and aspirin. Results: MCF-7 (mammary adenocarcinoma) cells down-regulated macrophage migration inhibitory factor (MIF), but tamoxifen-pretreated MCF-7 cells up-regulated MIF in co-cultured macrophages. Two molecular variants of MIF were observed in the co-cultured MCF-7 cells. Aspirin induced IL-10 expression in the macrophages, MCF-7 and tamoxifen-pretreated MCF-7 cells. Aspirin-pretreated macrophages potently induced IL-10 expression in the MCF-7 cells. Conclusion: Because MIF is a determinant of the M1 macrophage activation state, the MCF-7-induced ablation of MIF in TAMs is suggestive of partial M2 polarization. Tamoxifen modulates MCF-7 regulation of TAM gene expression and aspirin alters macrophage regulation of MCF-7 gene expression. Copyright© 2008 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved