Helicobacter pylori induced transactivation of SRE and AP-1 through the ERK signalling pathway in gastric cancer cells

Mitsuno, Yuzo

doi:10.1136/gut.49.1.18

Cited by 94 publications

(91 citation statements)

References 27 publications

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“…Therefore, we observed activation of the MAPK pathway in H. pylori-infected gastric epithelial cell lines, which led us to examine the effect of RGE administration on the changes in the MAPK pathway. Among three major subfamilies of MAPKs-extracellular signal regulated kinases (ERK), c-Jun N-terminal kinases (JNK), and p38-especially ERK was activated by H. pylori in this study similar to other investigatons (36), and ERK stimulation was inhibited by RGE in a dose dependent manner. These observations suggested that the cytoprotective action of RGE could be mediated by inactivation of the ERK pathway but not the JNK or p38 pathway.…”

Section: Discussionsupporting

confidence: 77%

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Rescue of Helicobacter pylori–Induced Cytotoxicity by Red Ginseng

et al. 2005

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Helicobacter pylori has been known to provoke gastric inflammation, ulceration, and DNA damage, based on which WHO defined H. pylori as a class I carcinogen. Although ginseng, the root of Panax ginseng C.A. Meyer, has been reported to possess antiadhesion or antimicrobial activity against H. pylori, in this study, we examined the protective effect of red ginseng extracts (RGE) against H. pylori-induced cytotoxicity and DNA damage. RGE significantly attenuated both H. pyloriinduced DNA damage assessed by comet assay and apoptosis measured by DNA fragmentation. Inactivation of ERK1/2 signaling and attenuation of caspase-3 activation and PARP cleavage were revealed with RGE against H. pylori infection. RGE decreased H. pylori-stimulated IL-8 gene expression, which resulted from the transcriptional regression of NF-κB. In conclusion, RGE showed significant gastroprotective effects against H. pylori-associated gastric mucosal cell damage, suggesting that red ginseng could be used as a medicinal phytonutrient against H. pylori infection.

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Section: Discussionsupporting

confidence: 77%

“…Among several signaling pathways, H. pylori induced transactivation of AP-1 through the ERK signaling pathway in gastric cancer cells (36). Therefore, we observed activation of the MAPK pathway in H. pylori-infected gastric epithelial cell lines, which led us to examine the effect of RGE administration on the changes in the MAPK pathway.…”

Section: Discussionmentioning

confidence: 97%

Rescue of Helicobacter pylori–Induced Cytotoxicity by Red Ginseng

et al. 2005

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“…Although H. pylori-stimulated gastric epithelial cell ERK activation has been reported, studies have differed regarding its CagA dependence (37)(38)(39)(40). Our data indicate both CagA-independent and -dependent processes.…”

Section: Discussionmentioning

confidence: 53%

“…In synovial fibroblasts, ERK activation mediates cytokine-and growth factor-stimulated MMP-1 secretion, enhancing tissue destruction in inflammatory arthritis (36). Although H. pylori stimulates ERK activation in gastric epithelial cells (37)(38)(39)(40)(41), the kinetics of ERK activation, as well as the role of CagA in this process, are not fully understood. H. pylori activation of gastric epithelial cell ERK may regulate both chemokine secretion and nuclear factor-B activation (42), contributing to proinflammatory responses.…”

mentioning

confidence: 99%

Helicobacter pylori Stimulates Gastric Epithelial Cell MMP-1 Secretion via CagA-dependent and -independent ERK Activation

Pillinger

Marjanović

Kim

et al. 2007

Journal of Biological Chemistry

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“…Post-transcriptionally, c-Jun activity is potentiated through phosphorylation of the transcriptional activator domain by SAPK/JNK. 27 H. pylori activated AP-1 through ERK signaling 22,28 and JNK signaling 29 in gastric epithelial cells. A variety of extracellular stimuli induce ras activation, resulting in activation of the ras/raf/ ERK kinase/MAPK cascade.…”

mentioning

confidence: 99%

Helicobacter pylori in a Korean isolate activates mitogen-activated protein kinases, AP-1, and NF-κB and induces chemokine expression in gastric epithelial AGS cells

et al. 2003

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Oxidant-sensitive transcription factors, nuclear factor-jB (NF-jB), and activator protein-1 (AP-1) have been considered as the regulators of inducible genes such as chemokines. Since oxygen radicals are considered as an important regulator in the pathogenesis of Helicobacter pylori (H. pylori)-induced gastric ulceration and carcinogenesis, chemokines such as interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) may be regulated by NF-jB and/or AP-1. Ras, the upstream activator for mitogen-activated protein kinase (MAPK) and MAPK cascade regulate AP-1 activation. The present study aims to investigate whether H. pylori in a Korean isolate (HP99) induces the expression of chemokines (IL-8, MCP-1), which is regulated by Ras, MAPK, AP-1, and NF-jB in gastric epithelial AGS cells, and whether these transcriptional regulations of chemokines are inhibited by transfection with mutant genes for Ras (ras N-17), c-Jun (TAM-67), and IjBa (MAD-3) or treatment with MAPK inhibitors (U0126 for extracellular signal-regulated kinase or SB203580 for p38 kinase). In addition, virulence factors of HP99 were characterized by PCR analysis for the isolated DNA. As a result, HP99 is identified as cagA þ , vacA s1b, m2, iceA1 H. pylori strain. HP99 induced a time-dependent expression of mRNA and protein for IL-8 and MCP-1 via mediation of MAPK, AP-1, and NF-jB. Transfection with mutant genes for Ras, c-Jun, and IjBa and treatment with MAPK inhibitors suppressed H. pylori-induced activation of transcription factors (NF-jB, AP-1) and expression of chemokines (IL-8, MCP-1) in AGS cells. In conclusion, Ras and MAPK cascade may act as the upstream signaling for the activation of AP-1 and NF-jB, which induce chemokine expression in H. pylori-infected AGS cells. Specific targeting of the activation of NF-jB and AP-1 may be effective for the prevention or treatment of gastric inflammation associated with H. pylori infection.

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Helicobacter pylori induced transactivation of SRE and AP-1 through the ERK signalling pathway in gastric cancer cells

Cited by 94 publications

References 27 publications

Rescue of Helicobacter pylori–Induced Cytotoxicity by Red Ginseng

Rescue of Helicobacter pylori–Induced Cytotoxicity by Red Ginseng

Helicobacter pylori Stimulates Gastric Epithelial Cell MMP-1 Secretion via CagA-dependent and -independent ERK Activation

Helicobacter pylori in a Korean isolate activates mitogen-activated protein kinases, AP-1, and NF-κB and induces chemokine expression in gastric epithelial AGS cells

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