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.
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.
Authors: Ge Jin; Hameem I Kawsar; Stanley A Hirsch; Chun Zeng; Xun Jia; Zhimin Feng; Santosh K Ghosh; Qing Yin Zheng; Aimin Zhou; Thomas M McIntyre; Aaron Weinberg Journal: PLoS One Date: 2010-06-08 Impact factor: 3.240
Authors: Pia S Zeiner; Corinna Preusse; Anna Golebiewska; Jenny Zinke; Ane Iriondo; Arnaud Muller; Tony Kaoma; Katharina Filipski; Monika Müller-Eschner; Simon Bernatz; Anna-Eva Blank; Peter Baumgarten; Elena Ilina; Anne Grote; Martin L Hansmann; Marcel A Verhoff; Kea Franz; Friedrich Feuerhake; Joachim P Steinbach; Jörg Wischhusen; Werner Stenzel; Simone P Niclou; Patrick N Harter; Michel Mittelbronn Journal: Brain Pathol Date: 2019-01-15 Impact factor: 6.508
Authors: Eva Verjans; Erik Noetzel; Nuran Bektas; Anke K Schütz; Hongqi Lue; Birgitt Lennartz; Arndt Hartmann; Edgar Dahl; Jürgen Bernhagen Journal: BMC Cancer Date: 2009-07-14 Impact factor: 4.430