Effect of lipopolysaccharide on toll-like receptor-4 signals in mouse cancer cells
Nasim Dana, Shaghayegh Haghjooy Javanmard, Golnaz Vaseghi
Abstract
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Nasim Dana, Shaghayegh Haghjooy Javanmard, Golnaz Vaseghi
Abstract
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BACKGROUND: Recent findings showed that activated TLR signals on cancer cells might promote cancer progression. This study was designed to explore the influence of Toll-like receptor 4 (TLR4) agonist lipopolysaccharides (LPS) on mouse melanoma and breast cancer cell proliferation and their TLR4 signalling. METHODS: Mouse melanoma cell line (B16F10) and breast cancer cell line (4T1) were taken as models. They were treated with LPS (0, 1.25, 2.5, 5, 7.5, 10 µg/ml) for 4, 16, 24, 48 h and MTT assay was done. The expression of TLR4, MyD88, NF-κB mRNA was detected by quantitative real time-polymerase chain reaction method quantitatively. RESULTS: Ultra-pure LPS at 5 µg/ml concentration increased significantly B16F10 cell viability 24 hour after stimulation, but not in 4T1 cell. The mRNA levels of TLR4, MyD88 and NF-κB were significantly up-regulated in both cell lines by stimulating the cells at 5 µg/ml LPS. CONCLUSIONS: Our data demonstrated that B16F10 and 4T1 cells are responsive to LPS, but their responses are time and dose dependent. These results provide new ways to understand the TLR4 signalling in tumour cells (Fig. 2, Ref. 24).
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BACKGROUND: Recent findings showed that activated TLR signals on cancer cells might promote cancer progression. This study was designed to explore the influence of Toll-like receptor 4 (TLR4) agonist lipopolysaccharides (LPS) on mouse melanoma and breast cancer cell proliferation and their TLR4 signalling. METHODS: Mouse melanoma cell line (B16F10) and breast cancer cell line (4T1) were taken as models. They were treated with LPS (0, 1.25, 2.5, 5, 7.5, 10 µg/ml) for 4, 16, 24, 48 h and MTT assay was done. The expression of TLR4, MyD88, NF-κB mRNA was detected by quantitative real time-polymerase chain reaction method quantitatively. RESULTS: Ultra-pure LPS at 5 µg/ml concentration increased significantly B16F10 cell viability 24 hour after stimulation, but not in 4T1 cell. The mRNA levels of TLR4, MyD88 and NF-κB were significantly up-regulated in both cell lines by stimulating the cells at 5 µg/ml LPS. CONCLUSIONS: Our data demonstrated that B16F10 and 4T1 cells are responsive to LPS, but their responses are time and dose dependent. These results provide new ways to understand the TLR4 signalling in tumour cells (Fig. 2, Ref. 24).
Key concepts: TLR4, Lipopolysaccharide, Toll-like receptor, Agonist, Cell culture, Cancer cell, Receptor, Cancer research