Regulation of HGF-mediated cell proliferation and invasion through NF-kappa B, JunB, and MMP-9 cascades in stomach cancer cells

Title
Regulation of HGF-mediated cell proliferation and invasion through NF-kappa B, JunB, and MMP-9 cascades in stomach cancer cells
Author(s)
이경희김재령[김재령]
Keywords
COLLAGENASE GENE-EXPRESSION; HEPATOCYTE GROWTH-FACTOR; HUMAN OVARIAN-CANCER; C-JUN; TRANSCRIPTION FACTORS; AP-1; KERATINOCYTES; TUMORIGENESIS; CARCINOMA; MATRIX-METALLOPROTEINASE-9
Issue Date
201203
Publisher
SPRINGER
Citation
CLINICAL & EXPERIMENTAL METASTASIS, v.29, no.3, pp.263 - 272
Abstract
Blocking of activator protein-1 activity leads to suppression of growth factor-induced transformation. However, the role of individual components of the Jun family in this process is unclear. Over-expression of JunB has been reported to be associated with neoplastic transformation and regulation of Matrix metalloproteinase-9 (MMP-9) expression. Using cDNA microarray, we found that JunB might be one of target genes up-regulated by hepatocyte growth factor (HGF). Therefore, we tried to investigate the role of JunB in HGF-medicated cell proliferation and cell invasion in human gastric cancer cells, NUGC3 and MKN28. We verified that HGF increased JunB in time and dose-dependent manners. The JunB levels were decreased by the treatment with an NF-kappa B inhibitor, pyrrolidine dithiocarbamate. Down-regulation of JunB by transfecting cells with JunB-short hairpin RNAs (shRNA) inhibited MMP-9 up-regulation induced by HGF. Furthermore, transfection with JunB-shRNA repressed HGF-mediated increases in cell proliferation and cell invasion. These data suggest that JunB might be regulated through an NF-kappa B pathway and up-regulation of JunB induced by HGF might play an important role in the regulation of cell proliferation and cell invasion through MMP-9 expression. In conclusion, these results may contribute to the JunB-associated malignant phenotype of gastric cancers by regulating MMP-9, and serve as a novel therapeutic target for stomach cancer therapy in the future.
URI
http://hdl.handle.net/YU.REPOSITORY/29491http://dx.doi.org/10.1007/s10585-011-9449-x
ISSN
0262-0898
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의과대학 > 내과학교실 > Articles
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