Citation
Kim, Mi H., et al. "Urokinase Plasminogen Activator Receptor Is Upregulated By Helicobacter Pylori in Human Gastric Cancer AGS Cells Via ERK, JNK, and AP-1." Biochemical and Biophysical Research Communications, vol. 333, no. 3, 2005, pp. 874-80.
Kim MH, Yoo HS, Chang HJ, et al. Urokinase plasminogen activator receptor is upregulated by Helicobacter pylori in human gastric cancer AGS cells via ERK, JNK, and AP-1. Biochem Biophys Res Commun. 2005;333(3):874-80.
Kim, M. H., Yoo, H. S., Chang, H. J., Hong, M. H., Kim, H. D., Chung, I. J., Shin, B. A., Cho, M. J., Ahn, B. W., & Jung, Y. D. (2005). Urokinase plasminogen activator receptor is upregulated by Helicobacter pylori in human gastric cancer AGS cells via ERK, JNK, and AP-1. Biochemical and Biophysical Research Communications, 333(3), 874-80.
Kim MH, et al. Urokinase Plasminogen Activator Receptor Is Upregulated By Helicobacter Pylori in Human Gastric Cancer AGS Cells Via ERK, JNK, and AP-1. Biochem Biophys Res Commun. 2005 Aug 5;333(3):874-80. PubMed PMID: 15963460.
TY - JOUR
T1 - Urokinase plasminogen activator receptor is upregulated by Helicobacter pylori in human gastric cancer AGS cells via ERK, JNK, and AP-1.
AU - Kim,Mi H,
AU - Yoo,Hyung S,
AU - Chang,Hee J,
AU - Hong,Min H,
AU - Kim,Ho D,
AU - Chung,Ik J,
AU - Shin,Boo A,
AU - Cho,Myung J,
AU - Ahn,Bong W,
AU - Jung,Young D,
PY - 2005/05/04/received
PY - 2005/06/01/accepted
PY - 2005/6/21/pubmed
PY - 2005/9/27/medline
PY - 2005/6/21/entrez
SP - 874
EP - 80
JF - Biochemical and biophysical research communications
JO - Biochem Biophys Res Commun
VL - 333
IS - 3
N2 - The gastric pathogen Helicobacter pylori (H. pylori) is suggested to be associated with gastric cancer progression. In this study, we investigated the effect of H. pylori on urokinase plasminogen activator receptor (uPAR) expression which has been known to correlate closely with gastric cancer invasion. H. pylori induced the uPAR expression in a time- and concentration-dependent manner. Specific inhibitors and inactive mutants of MEK-1 and JNK were found to suppress the H. pylori-induced uPAR expression and the uPAR promoter activity. Electrophoretic mobility shift assay and transient transfection study using an AP-1 decoy oligonucleotide confirmed that the activation of AP-1 is involved in the H. pylori-induced uPAR upregulation. The AGS cells treated with H. pylori showed a remarkably enhanced invasiveness, and this effect was partially abrogated by uPAR-neutralizing antibodies. These results suggest that H. pylori induces uPAR expression via Erk-1/2, JNK, and AP-1 signaling pathways and, in turn, stimulates the cell invasiveness in human gastric cancer AGS cells.
SN - 0006-291X
UR - https://www.unboundmedicine.com/medline/citation/15963460/Urokinase_plasminogen_activator_receptor_is_upregulated_by_Helicobacter_pylori_in_human_gastric_cancer_AGS_cells_via_ERK_JNK_and_AP_1_
L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(05)01177-0
DB - PRIME
DP - Unbound Medicine
ER -