IL-1 beta-stimulated urokinase plasminogen activator expression through NF-kappa B in gastric cancer after HGF treatment
- IL-1 beta-stimulated urokinase plasminogen activator expression through NF-kappa B in gastric cancer after HGF treatment
- 이경희; 최은영; 고성애; 김민경; 장병익; 김상운; 김재룡
- HELICOBACTER-PYLORI INFECTION; CARCINOMA CELLS; INFLAMMATORY CYTOKINES; GENE-EXPRESSION; LUNG-CANCER; INTERLEUKIN-1-BETA; SYSTEM; TUMORIGENESIS; INVASIVENESS; ANGIOGENESIS
- Issue Date
- SPANDIDOS PUBL LTD
- ONCOLOGY REPORTS, v.31, no.5, pp.2123 - 2130
- The potential of hepatocyte growth factor (HGF) to regulate the expression of urokinase plasminogen activator (uPA) in a gastric cancer cell is not widely acknowledged. To identify the genes associated with the plasminogen activator proteolytic axis by HGF, we used cDNA microarray technology and selected genes upregulated or downregulated in two gastric cell lines (NUGC-3 and MKN-28). First, IL-1 beta RNA and protein were confirmed to be upregulated. Then, we investigated the effect of IL-1 beta induced by HGF on the uPA system, facilitating the migration and invasion of cancer cells in the metastatic process. The role for IL-1 beta in HGF-induced upregulation of uPA was determined by knockdown of IL-1 beta with IL-1 beta shRNA and a chromatin immune precipitation assay. The levels of IL-1 beta and uPA were upregulated in cells treated with HGF in a dose-dependent manner. HGF-induced upregulation of uPA was suppressed by IL-1 beta knockdown. HGF enhanced the binding activity of NF-kappa B to the uPA promoter in control cells, but not in the IL-1 beta shRNA cells. We confirmed the functional role of HGF inactivation of the uPA promoter by a reporter gene assay. Downregulation of IL-1 beta using IL-1 beta shRNA also decreased cell proliferation and in vitro cell invasion. IL-1 beta stimulated uPA expression through ERK and NF-kappa B in gastric cancer, which may therefore be promising targets for gastric cancer therapy.
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