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Store-operated Ca(2+) Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells
Helicobacter pylori has been identified as one of the major causes of chronic gastritis, gastric and duodenal ulcers, and gastric cancer. Lipopolysaccharide (LPS) is a major component of the outer membrane of gram-negative bacteria, and H. pylori LPS might play an exclusively important role in activ...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5643532/ https://www.ncbi.nlm.nih.gov/pubmed/29038542 http://dx.doi.org/10.1038/s41598-017-12648-1 |
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author | Wong, Jhen-Hong Ho, Kuo-Hao Nam, Sean Hsu, Wen-Li Lin, Chia-Hsien Chang, Che-Mai Wang, Jaw-Yuan Chang, Wei-Chiao |
author_facet | Wong, Jhen-Hong Ho, Kuo-Hao Nam, Sean Hsu, Wen-Li Lin, Chia-Hsien Chang, Che-Mai Wang, Jaw-Yuan Chang, Wei-Chiao |
author_sort | Wong, Jhen-Hong |
collection | PubMed |
description | Helicobacter pylori has been identified as one of the major causes of chronic gastritis, gastric and duodenal ulcers, and gastric cancer. Lipopolysaccharide (LPS) is a major component of the outer membrane of gram-negative bacteria, and H. pylori LPS might play an exclusively important role in activating inflammatory pathways in monocytes and macrophages. To study the role of LPS in the underlying mechanism of inflammatory responses, we established an in vitro model using the human AGS gastric cancer cell line. We found that LPS mediates inflammation through setting off a cascade of events: activation of the store-operated calcium (SOC) channel, initiation of downstream NF-κB signaling, and phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). Phosphorylated ERK1/2 promotes the nuclear translocation of NF-κB, and eventually elevates the expression level of COX-2, a major inflammatory gene. |
format | Online Article Text |
id | pubmed-5643532 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-56435322017-10-19 Store-operated Ca(2+) Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells Wong, Jhen-Hong Ho, Kuo-Hao Nam, Sean Hsu, Wen-Li Lin, Chia-Hsien Chang, Che-Mai Wang, Jaw-Yuan Chang, Wei-Chiao Sci Rep Article Helicobacter pylori has been identified as one of the major causes of chronic gastritis, gastric and duodenal ulcers, and gastric cancer. Lipopolysaccharide (LPS) is a major component of the outer membrane of gram-negative bacteria, and H. pylori LPS might play an exclusively important role in activating inflammatory pathways in monocytes and macrophages. To study the role of LPS in the underlying mechanism of inflammatory responses, we established an in vitro model using the human AGS gastric cancer cell line. We found that LPS mediates inflammation through setting off a cascade of events: activation of the store-operated calcium (SOC) channel, initiation of downstream NF-κB signaling, and phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). Phosphorylated ERK1/2 promotes the nuclear translocation of NF-κB, and eventually elevates the expression level of COX-2, a major inflammatory gene. Nature Publishing Group UK 2017-10-16 /pmc/articles/PMC5643532/ /pubmed/29038542 http://dx.doi.org/10.1038/s41598-017-12648-1 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Wong, Jhen-Hong Ho, Kuo-Hao Nam, Sean Hsu, Wen-Li Lin, Chia-Hsien Chang, Che-Mai Wang, Jaw-Yuan Chang, Wei-Chiao Store-operated Ca(2+) Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells |
title | Store-operated Ca(2+) Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells |
title_full | Store-operated Ca(2+) Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells |
title_fullStr | Store-operated Ca(2+) Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells |
title_full_unstemmed | Store-operated Ca(2+) Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells |
title_short | Store-operated Ca(2+) Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells |
title_sort | store-operated ca(2+) entry facilitates the lipopolysaccharide-induced cyclooxygenase-2 expression in gastric cancer cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5643532/ https://www.ncbi.nlm.nih.gov/pubmed/29038542 http://dx.doi.org/10.1038/s41598-017-12648-1 |
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