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G 蛋白偶联雌激素受体可预防幽门螺杆菌细胞毒素相关基因 A 激活胃癌细胞中的核因子-κB 启动子。

G-protein-coupled estrogen receptor prevents nuclear factor-kappa B promoter activation by Helicobacter pylori cytotoxin-associated gene A in gastric cancer cells.

机构信息

Laboratory of Immunology and Infection Control, Department of Veterinary Medicine, School of Veterinary Medicine, Azabu University, Kanagawa, Japan.

Institute of Gene Research, Yamaguchi University Science Research Center, Yamaguchi, Japan.

出版信息

J Vet Med Sci. 2023 Dec 27;85(12):1348-1354. doi: 10.1292/jvms.23-0054. Epub 2023 Nov 13.

DOI:10.1292/jvms.23-0054
PMID:37952974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10788165/
Abstract

Helicobacter pylori is a well-known pathogen that causes chronic gastritis, leading to the development of gastric cancer. This bacterium has also been detected in dogs, and symptoms similar to those in humans have been reported. The cytotoxin-associated gene A (CagA) is involved in pathogenesis through aberrant activation of host signal transduction, including the nuclear factor-kappa B (NF-κB) pathway. We have previously shown the anti-inflammatory effect of the G-protein-coupled estrogen receptor (GPER) via inhibiting of NF-κB activation in several cells. Therefore, here, we investigated the effect of GPER on CagA-mediated NF-κB promoter activity and showed that CagA overexpression in gastric cancer cells activated the NF-κB reporter and induced interleukin 8 (il-8) expression, both of which were inhibited by the GPER agonist.

摘要

幽门螺杆菌是一种众所周知的病原体,可导致慢性胃炎,并引发胃癌。这种细菌也存在于狗体内,并报告了类似人类的症状。细胞毒素相关基因 A (CagA) 通过异常激活宿主信号转导,包括核因子-κB (NF-κB) 途径,参与发病机制。我们之前已经证明了 G 蛋白偶联雌激素受体 (GPER) 通过抑制几种细胞中的 NF-κB 激活具有抗炎作用。因此,在这里,我们研究了 GPER 对 CagA 介导的 NF-κB 启动子活性的影响,并表明胃癌细胞中 CagA 的过表达激活了 NF-κB 报告基因,并诱导白细胞介素 8 (il-8) 的表达,这两者均被 GPER 激动剂抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de25/10788165/88fe9537f307/jvms-85-1348-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de25/10788165/9dfa95c360d3/jvms-85-1348-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de25/10788165/1f90a150e3f9/jvms-85-1348-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de25/10788165/89de3a504244/jvms-85-1348-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de25/10788165/88fe9537f307/jvms-85-1348-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de25/10788165/9dfa95c360d3/jvms-85-1348-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de25/10788165/1f90a150e3f9/jvms-85-1348-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de25/10788165/89de3a504244/jvms-85-1348-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de25/10788165/88fe9537f307/jvms-85-1348-g004.jpg

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