Store-operated Ca2+ Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells

被引：0
作者：
Jhen-Hong Wong
Kuo-Hao Ho
Sean Nam
Wen-Li Hsu
Chia-Hsien Lin
Che-Mai Chang
Jaw-Yuan Wang
Wei-Chiao Chang
机构：
[1] Department of Clinical Pharmacy,
[2] School of Pharmacy,undefined
[3] Taipei Medical University,undefined
[4] Department of Clinical Pharmacy,undefined
[5] Master Program for Clinical Pharmacogenomics and Pharmacoproteomics,undefined
[6] School of Pharmacy,undefined
[7] Taipei Medical University,undefined
[8] Department of Pharmacy,undefined
[9] Wan Fang Hospital,undefined
[10] Taipei Medical University,undefined
[11] Cancer Center,undefined
[12] Kaohsiung Medical University Hospital,undefined
[13] Center for Biomarkers and Biotech Drugs,undefined
[14] Kaohsiung Medical University,undefined
[15] Division of Colorectal Surgery,undefined
[16] Department of Surgery,undefined
[17] Kaohsiung Medical University Hospital,undefined
[18] Kaohsiung Medical University,undefined
[19] Graduate Institute of Clinical Medicine,undefined
[20] College of Medicine,undefined
[21] Kaohsiung Medical University,undefined
[22] Department of Surgery,undefined
[23] Faculty of Medicine,undefined
[24] College of Medicine,undefined
[25] Kaohsiung Medical University,undefined
[26] Department of Health Industry Management,undefined
[27] School of Health Care Management,undefined
[28] Kainan University,undefined
来源：
Scientific Reports | / 7卷
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摘要：
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.
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