PMID- 18357389
OWN - NLM
STAT- MEDLINE
DCOM- 20080521
LR  - 20161124
IS  - 1021-335X (Print)
IS  - 1021-335X (Linking)
VI  - 19
IP  - 4
DP  - 2008 Apr
TI  - Activation of matrix metalloproteinase-9 by TNF-alpha in human urinary bladder 
      cancer HT1376 cells: the role of MAP kinase signaling pathways.
PG  - 1007-13
AB  - The expression of matrix metalloproteinase-9 (MMP-9) has been implicated in tumor 
      invasion and metastasis. In this study, the factors and signaling pathways that 
      are involved in the regulation of the MMP-9 expression were examined in urinary 
      bladder cancer HT1376 cells. Tumor necrosis factor-alpha (TNF-alpha) stimulated 
      the secretion of MMP-9 in HT1376 cells, as shown by zymography and immunoblot 
      analysis. At the level of transcription, TNF-alpha also stimulated 5'-flanking 
      promoter activity of MMP-9. Transcription factor NF-kappaB, AP-1 and Sp-1 binding 
      sites were identified by a gel shift assay to be cis-elements for TNF-alpha 
      activation of the MMP-9 promoter. TNF-alpha activates multiple signaling pathways 
      in HT1376 cells, including the extracellular signal-regulated kinase (ERK1/2), 
      p38 MAP kinase and JNK pathways. Chemical inhibitors, which specifically inhibit 
      each of these TNF-alpha-activated pathways, were used to examine the signaling 
      pathways involved in TNF-alpha-mediated MMP-9 expression. The ERK1/2 inhibitor, 
      U0126 and the p38 MAP kinase inhibitor, SB203580, significantly down-regulated 
      TNF-alpha-induced MMP-9 expression and promoter activity. The transactivation of 
      TNF-alpha-stimulated NF-kappaB, AP-1 and Sp-1 were inhibited by U0126 and 
      SB203580 treatment. In conclusion, the findings of the present study indicate 
      that TNF-alpha induces MMP-9 expression in HT1376 cells by activating 
      transcription factors, which are involved in the ERK1/2- and p38 MAP 
      kinase-mediated control of MMP-9 regulation, namely, NF-kappaB, AP-1 and Sp-1.
FAU - Lee, Se-Jung
AU  - Lee SJ
AD  - Department of Food and Biotechnology, Chungju National University, Chungbuk 
      380-702, Korea.
FAU - Park, Sung-Soo
AU  - Park SS
FAU - Cho, Young-Hwa
AU  - Cho YH
FAU - Park, Keerang
AU  - Park K
FAU - Kim, Eun-Jung
AU  - Kim EJ
FAU - Jung, Kyung-Hwan
AU  - Jung KH
FAU - Kim, Si-Kwan
AU  - Kim SK
FAU - Kim, Wun-Jae
AU  - Kim WJ
FAU - Moon, Sung-Kwon
AU  - Moon SK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (Butadienes)
RN  - 0 (Imidazoles)
RN  - 0 (Nitriles)
RN  - 0 (Pyridines)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (U 0126)
RN  - 9007-49-2 (DNA)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
RN  - OU13V1EYWQ (SB 203580)
SB  - IM
MH  - Butadienes/pharmacology
MH  - Cell Line, Tumor
MH  - DNA/metabolism
MH  - Enzyme Activation
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Humans
MH  - Imidazoles/pharmacology
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - MAP Kinase Signaling System/*physiology
MH  - Matrix Metalloproteinase 9/genetics/*metabolism
MH  - Nitriles/pharmacology
MH  - Promoter Regions, Genetic
MH  - Pyridines/pharmacology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Urinary Bladder Neoplasms/*enzymology
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2008/03/22 09:00
MHDA- 2008/05/22 09:00
CRDT- 2008/03/22 09:00
PHST- 2008/03/22 09:00 [pubmed]
PHST- 2008/05/22 09:00 [medline]
PHST- 2008/03/22 09:00 [entrez]
PST - ppublish
SO  - Oncol Rep. 2008 Apr;19(4):1007-13.