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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 05; 333(3):874-80.BB

Abstract

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.

Authors+Show Affiliations

Chonnam University Research Institute of Medical Sciences, Chonnam National University Medical School, Kwangju 501-190, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15963460

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.
* Article titles in AMA citation format should be in sentence-case
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 -