Helicobacter pylori virulence factor CagA promotes tumorigenesis of gastric cancer via multiple signaling pathways

Xin, Yong; Tang, Bo; Li, Bosheng; Xie, Rui; Hu, C.; Luo, Gang; Qin, Yong; Dong, Hui; Yang, Shi‐Ming

doi:10.1186/s12964-015-0111-0

Cited by 172 publications

(138 citation statements)

References 111 publications

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“…The level of this key tumor suppressor is increased following infection with CagA-positive H. pylori strains and decreased rapidly during H. pylori eradication [10], whereas a continuous bacterial infection caused a persistently high level of p53. This phenomenon may be driven by the DNA damage related to inflammatory processes [11]. …”

Section: Caga-positive H Pylori Strains-related Diseases (Figure 1)mentioning

confidence: 99%

The Role ofH. pyloriCagA in Regulating Hormones of Functional Dyspepsia Patients

Meng

Wang

Deng

et al. 2016

Gastroenterology Research and Practice

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Helicobacter pylori (H. pylori, Hp) colonizes the stomachs of approximately 20%–80% of humans throughout the world. The Word Healthy Organization (WHO) classified H. pylori as a group 1 carcinogenic factor in 1994. Recently, an increasing number of studies has shown an association between H. pylori infection and various extragastric diseases. Functional dyspepsia (FD) is considered a biopsychosocial disorder with multifactorial pathogenesis, and studies have shown that infection with CagA-positive H. pylori strains could explain some of the symptoms of functional dyspepsia. Moreover, CagA-positive H. pylori strains have been shown to affect the secretion of several hormones, including 5-HT, ghrelin, dopamine, and gastrin, and altered levels of these hormones might be the cause of the psychological disorders of functional dyspepsia patients. This review describes the mutual effects of H. pylori and hormones in functional dyspepsia and provides new insight into the pathogenesis of functional dyspepsia.

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Section: Caga-positive H Pylori Strains-related Diseases (Figure 1)mentioning

confidence: 99%

The Role ofH. pyloriCagA in Regulating Hormones of Functional Dyspepsia Patients

Meng

Wang

Deng

et al. 2016

Gastroenterology Research and Practice

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“…Given the striking association between H. pylori and GC, decades of research has sought to determine the molecular mechanisms underlying H. pylori -associated cancer development. Indeed, numerous molecular pathways have been identified as targets of this pathogen (reviewed in [5, 6]). Recent reports have revealed several H. pylori -targeted pathways that are also altered in various forms of cancer.…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanisms of gastric cancer initiation and progression by Helicobacter pylori

Servetas

Bridge²,

Merrell³

2016

Current Opinion in Infectious Diseases

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Purpose of Review Infection with the Gram-negative, microaerophilic pathogen Helicobacter pylori results in gastric cancer (GC) in a subset of infected individuals. As such, H. pylori is the only World Health Organization classified bacterial class I carcinogen. Numerous studies have identified mechanisms by which H. pylori alters host cell signaling pathways to cause disease. The purpose of this review is to highlight recent studies that explore mechanisms associated with induction of GC. Recent Findings Over the last year and a half, new mechanisms contributing to the etiology of H. pylori associated GC development have been discovered. In addition to utilizing the oncogenic CagA toxin to alter host cell signaling pathways, H. pylori also induces host DNA damage and alters DNA methylation to perturb downstream signaling. Furthermore, H. pylori activates numerous host cell pathways and proteins that result in epithelial-to-mesenchymal transition (EMT) and induction of cell survival and proliferation. Summary Mounting evidence suggests that H. pylori promotes gastric carcinogenesis using a multifactorial approach. Intriguingly, many of the targeted pathways and mechanism show commonality with diverse forms of cancer.

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“…It has been estimated that 50 % of global population are infected with H. pylori due to its highly contagious nature (Yong et al, 2015). The pathogenesis of H. pylori infection is extremely complex owing to its multi-virulence factors like Cytotoxin-associated gene A (CagA), Cag pathogenicity island (Cag PAI), lipopolysaccharide (LPS), urease and Vacuolating cytotoxin A (VacA).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory Activity of Mangiferin on Helicobacter Pylori-Induced Inflammation in Human Gastric Carcinoma Ags Cells

Zhang¹,

Yue²

2016

AJTCAM

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Background: Gastric cancer is a serious health issue caused by H. pylori and claims more lives in developing and undeveloped countries. Hence, the need for a natural drug with several pharmacological activities with no adverse effect are highly recommended. The target of this study was to verify the anti-H. pyloric efficacy of mangiferin (MF) on H. pyloriinfected AGS cells. Materials and methods: AGS cells were co-cultured with H. pylori and incubated with increased concentration of MF (10, 20, 50 and 100 µg/mL) or amoxicillin (AMX) and DMSO (control) group to assess its anti-H. pyloric effect by checking inhibitory zone, bacterial drug sensitivity test (MIC and MBC), adhesion and invasive property and various inflammatory markers. Results: Co-culturing of H. pylori-infected AGS cells with MF (100 µg) considerably increased (p<0.05) the inhibitory zone as well as substantially lowered (p<0.05) in the levels of MBC and MIC with decreased adhesion and invasive property in a dose-dependent manner and thus endorsing its anti H. pyloric activity and are almost equivalent to antibiotic AMX. Meanwhile, inflammatory markers such as NF-κB subunit p65, interleukins-1β, IL-8, and TNF-α were also markedly suppressed (p<0.01) on treatment with MF. In addition, the protein expression of inflammatory enzymes like COX-2 and iNOS were notably downregulated (p<0.05) in AGS cells incubated with MF. Conclusion: We, concluded that MF treatment with H. pylori-infected AGS cells significantly suppressed the adhesion and invasion process as well as deactivated NF-p65 thereby blocking inflammatory response and thus lower the incidence of gastric carcinoma.

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Helicobacter pylori virulence factor CagA promotes tumorigenesis of gastric cancer via multiple signaling pathways

Cited by 172 publications

References 111 publications

The Role ofH. pyloriCagA in Regulating Hormones of Functional Dyspepsia Patients

The Role ofH. pyloriCagA in Regulating Hormones of Functional Dyspepsia Patients

Molecular mechanisms of gastric cancer initiation and progression by Helicobacter pylori

Inhibitory Activity of Mangiferin on Helicobacter Pylori-Induced Inflammation in Human Gastric Carcinoma Ags Cells

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