@article{f48e9c2025d1405eb1ea325de54fb01a,
title = "Store-operated Ca2+ Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells",
abstract = "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.",
author = "Wong, {Jhen Hong} and Ho, {Kuo Hao} and Sean Nam and Hsu, {Wen Li} and Lin, {Chia Hsien} and Chang, {Che Mai} and Wang, {Jaw Yuan} and Chang, {Wei Chiao}",
note = "Funding Information: This research was supported by grants from the Excellence for Cancer Research Center Grant through funding by the Ministry of Science and Technology (MOST105-2325-B-037-001) and the Ministry of Health and Welfare (MOHW106-TDU-B-212-144007), Health and welfare surcharge of tobacco products, Taiwan, Republic of China as well as grants from Kaohsiung Medical University Hospital (KMUH105-5R26, KMUHS10601, KMUHS10608, KMUHA10664), and the Grant of Biosignature in Colorectal Cancers, Academia Sinica, Taiwan. Publisher Copyright: {\textcopyright} 2017 The Author(s).",
year = "2017",
month = dec,
day = "1",
doi = "10.1038/s41598-017-12648-1",
language = "English",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",
number = "1",
}