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      TLR4 signaling induces B7-H1 expression through MAPK pathways in bladder cancer cells.

      Cancer Investigation
      Anthracenes, pharmacology, Antigens, CD, biosynthesis, genetics, Antigens, CD14, physiology, Antigens, CD274, Carcinoma, Transitional Cell, metabolism, pathology, Cell Line, Tumor, Chromones, Extracellular Signal-Regulated MAP Kinases, antagonists & inhibitors, Flavonoids, Humans, Imidazoles, JNK Mitogen-Activated Protein Kinases, Lipopolysaccharides, MAP Kinase Signaling System, drug effects, Morpholines, Neoplasm Proteins, Phosphatidylinositol 3-Kinases, Phosphorylation, Protein Kinase Inhibitors, Protein Processing, Post-Translational, Proto-Oncogene Proteins c-akt, Pyridines, Toll-Like Receptor 4, Up-Regulation, Urinary Bladder Neoplasms

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          Abstract

          TLR4 (Toll-like receptor 4) and B7-H1, which were known to be restricted to immune cells in the past, were found to be aberrantly expressed in a majority of tumor cells, facilitating tumor evasion from immune surveillance. Our study demonstrated that activation of TLR4 signaling in bladder cancer cells up-regulated B7-H1 expression. Furthermore, this regulation was significantly attenuated by ERK or JNK inhibitor. Our results elucidated the molecule mechanism of regulation of B7-H1 expression through TLR4 signaling and may suggest new strategies of down-regulating the cancer-associated B7-H1 expression for bladder cancer treatment.

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