The effects of lipopolysaccharides, imiquimod, and emodin on adherence of macrophages to breast cancer cells and the production of tumor necrosis factor alpha (TNFα) by macrophages
2015
- 29Usage
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Artifact Description
The purpose of this study was to gain a more comprehensive understanding of the potential usefulness of lipopolysaccharides (LPS), imiquimod and emodin as anti-cancer therapies. It was hypothesized that lipopolysaccharides, imiquimod, and emodin may affect macrophages’ ability in fighting cancer cells by influencing macrophage-cancer cell adhesion and the production of pro-tumor cytokine tumor necrosis factor alpha (TNFα), two mechanisms by which macrophages may promote cancer cell growth, invasion and metastasis. In the study, lipopolysaccharides (LPS), imiquimod, and emodin were used to treat macrophages at the concentrations nontoxic to the cells. Twenty-four wells of cultured macrophages were evenly divided up into four groups, and each group was treated with 100 ng/ml LPS, 1000 ng/ml imiquimod, 10 μM emodin, or vehicle. The medium was collected for ELISA. EO771-GFP breast cancer cells were then added to the macrophages for 1 hour, and the non-adherent cells were washed away. The plates were examined under a fluorescence microscope, and the adhered EO771-GFP cells were counted. An ANOVA determined that the counts among the groups were significantly different; F(3,28)=7.07, p<0.05, and in particular, imiquimod and emodin significantly reduced macrophage-cancer cell adhesion. ELISA was performed to measure TNFα concentrations in the macrophage medium. An ANOVA determined that the concentrations were significantly different; F(3,28)=85.29, p<0.05, and importantly, emodin substantially inhibited TNFα production by macrophages. In conclusion, the hypothesis was supported, and emodin was found to be the best treatment because it reduced the cancer cell-macrophage adhesion as well as the TNFα production by macrophages.
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