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Title: Induction of COX-2 protein expression by vanadate in A549 human lung carcinoma cell line through EGF receptor and p38 MAPK-mediated pathway

Abstract

Vanadate is a transition metal widely distributed in the environment. It has been reported that vanadate associated with air pollution particles can modify DNA synthesis, causing cell growth arrest, and apoptosis. Moreover, vanadium exposure was also found to cause the synthesis of inflammatory cytokines, such as interleukin-1, tumor necrosis factor-{alpha}, and prostaglandin E{sub 2}. Here, we found that exposure of A549 human lung carcinoma cells to vanadate led to extracellular signal-regulated kinase, c-Jun NH{sub 2}-terminal protein kinases (JNKs), p38 mitogen-activated protein kinase (p38) activation, and COX-2 protein expression in a dose-dependent manner. SB203580, a p38 MAPK inhibitor, but not PD098059 and SP600125, specific inhibitor of MKK1 and selective inhibitor of JNK, respectively, suppressed COX-2 expression. Furthermore, the epithelial growth factor (EGF) receptor specific inhibitor (PD153035) reduced vanadate-induced COX-2 expression. However, scavenging of vanadate-induced reactive oxygen species by catalase, a specific H{sub 2}O{sub 2} inhibitor, or DPI, an NADPH oxidase inhibitor, resulted in no inhibition on COX-2 expression. Together, we suggested that EGF receptor and p38 MAPK signaling pathway may be involved in vanadate-induced COX-2 protein expression in A549 human lung carcinoma cell line.

Authors:
 [1];  [1];  [2];  [3]
  1. Institute of Biotechnology, National Cheng Kung University, No. 1 University Rd. 701, Tainan, Taiwan (China)
  2. (China)
  3. Institute of Biotechnology, National Cheng Kung University, No. 1 University Rd. 701, Tainan, Taiwan (China) and Department of Life Sciences, National Cheng Kung University, No. 1 University Rd. 701, Tainan, Taiwan (China). E-mail: haojen@mail.ncku.edu.tw
Publication Date:
OSTI Identifier:
20798745
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 339; Journal Issue: 2; Other Information: DOI: 10.1016/j.bbrc.2005.11.045; PII: S0006-291X(05)02540-4; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; AIR POLLUTION; APOPTOSIS; BIOSYNTHESIS; CARCINOMAS; CATALASE; DNA; HYDROGEN PEROXIDE; INFLAMMATION; INHIBITION; LUNGS; LYMPHOKINES; OXIDASES; PHOSPHOTRANSFERASES; PROSTAGLANDINS; RECEPTORS; VANADIUM

Citation Formats

Chien, P.-S., Mak, O.-T., Department of Life Sciences, National Cheng Kung University, No. 1 University Rd. 701, Tainan, Taiwan, and Huang, H.-J.. Induction of COX-2 protein expression by vanadate in A549 human lung carcinoma cell line through EGF receptor and p38 MAPK-mediated pathway. United States: N. p., 2006. Web. doi:10.1016/j.bbrc.2005.11.045.
Chien, P.-S., Mak, O.-T., Department of Life Sciences, National Cheng Kung University, No. 1 University Rd. 701, Tainan, Taiwan, & Huang, H.-J.. Induction of COX-2 protein expression by vanadate in A549 human lung carcinoma cell line through EGF receptor and p38 MAPK-mediated pathway. United States. doi:10.1016/j.bbrc.2005.11.045.
Chien, P.-S., Mak, O.-T., Department of Life Sciences, National Cheng Kung University, No. 1 University Rd. 701, Tainan, Taiwan, and Huang, H.-J.. Fri . "Induction of COX-2 protein expression by vanadate in A549 human lung carcinoma cell line through EGF receptor and p38 MAPK-mediated pathway". United States. doi:10.1016/j.bbrc.2005.11.045.
@article{osti_20798745,
title = {Induction of COX-2 protein expression by vanadate in A549 human lung carcinoma cell line through EGF receptor and p38 MAPK-mediated pathway},
author = {Chien, P.-S. and Mak, O.-T. and Department of Life Sciences, National Cheng Kung University, No. 1 University Rd. 701, Tainan, Taiwan and Huang, H.-J.},
abstractNote = {Vanadate is a transition metal widely distributed in the environment. It has been reported that vanadate associated with air pollution particles can modify DNA synthesis, causing cell growth arrest, and apoptosis. Moreover, vanadium exposure was also found to cause the synthesis of inflammatory cytokines, such as interleukin-1, tumor necrosis factor-{alpha}, and prostaglandin E{sub 2}. Here, we found that exposure of A549 human lung carcinoma cells to vanadate led to extracellular signal-regulated kinase, c-Jun NH{sub 2}-terminal protein kinases (JNKs), p38 mitogen-activated protein kinase (p38) activation, and COX-2 protein expression in a dose-dependent manner. SB203580, a p38 MAPK inhibitor, but not PD098059 and SP600125, specific inhibitor of MKK1 and selective inhibitor of JNK, respectively, suppressed COX-2 expression. Furthermore, the epithelial growth factor (EGF) receptor specific inhibitor (PD153035) reduced vanadate-induced COX-2 expression. However, scavenging of vanadate-induced reactive oxygen species by catalase, a specific H{sub 2}O{sub 2} inhibitor, or DPI, an NADPH oxidase inhibitor, resulted in no inhibition on COX-2 expression. Together, we suggested that EGF receptor and p38 MAPK signaling pathway may be involved in vanadate-induced COX-2 protein expression in A549 human lung carcinoma cell line.},
doi = {10.1016/j.bbrc.2005.11.045},
journal = {Biochemical and Biophysical Research Communications},
number = 2,
volume = 339,
place = {United States},
year = {Fri Jan 13 00:00:00 EST 2006},
month = {Fri Jan 13 00:00:00 EST 2006}
}