Current information on the association of <i>Helicobacter pylori</i> with autophagy and gastric cancer

Eslami, Majid; Yousefi, Bahman; Kokhaei, Parviz; Arabkari, Vahid; Ghasemian, Abdolmajid

doi:10.1002/jcp.28279

Cited by 40 publications

(29 citation statements)

References 66 publications

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“…During carcinogenesis, autophagy acts as a tumor suppressor by decomposing damaged organelles and increasing genomic stability [ 41 ]. The virulence factor of H. pylori , vacA , induces autophagy that protects cells by restricting toxin-induced cell damage in short-term exposure [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Effect of Astaxanthin on Activation of Autophagy and Inhibition of Apoptosis in Helicobacter pylori-Infected Gastric Epithelial Cell Line AGS

2020

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Helicobacter pylori (H. pylori) infection leads to the massive apoptosis of the gastric epithelial cells, causing gastric ulcers, gastritis, and gastric adenocarcinoma. Autophagy is a cellular recycling process that plays important roles in cell death decisions and can protect cells by preventing apoptosis. Upon the induction of autophagy, the level of the autophagy substrate p62 is reduced and the autophagy-related ratio of microtubule-associated proteins 1A/1B light chain 3B (LC3B)-II/LC3B-I is heightened. AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) are involved in the regulation of autophagy. Astaxanthin (AST) is a potent anti-oxidant that plays anti-inflammatory and anti-cancer roles in various cells. In the present study, we examined whether AST inhibits H. pylori-induced apoptosis through AMPK-mediated autophagy in the human gastric epithelial cell line AGS (adenocarcinoma gastric) in vitro. In this study, H. pylori induced apoptosis. Compound C, an AMPK inhibitor, enhanced the H. pylori-induced apoptosis of AGS cells. In contrast, metformin, an AMPK activator, suppressed H. pylori-induced apoptosis, showing that AMPK activation inhibits H. pylori-induced apoptosis. AST inhibited H. pylori-induced apoptosis by increasing the phosphorylation of AMPK and decreasing the phosphorylation of RAC-alpha serine/threonine-protein kinase (Akt) and mTOR in H. pylori-stimulated cells. The number of LC3B puncta in H. pylori-stimulated cells increased with AST. These results suggest that AST suppresses the H. pylori-induced apoptosis of AGS cells by inducing autophagy through the activation of AMPK and the downregulation of its downstream target, mTOR. In conclusion, AST may inhibit gastric diseases associated with H. pylori infection by increasing autophagy through the activation of the AMPK pathway.

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Section: Discussionmentioning

confidence: 99%

Effect of Astaxanthin on Activation of Autophagy and Inhibition of Apoptosis in Helicobacter pylori-Infected Gastric Epithelial Cell Line AGS

2020

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“…The human gastric microbiome would be related to gastric diseases, but reports about the microbial composition of GJ and tissues in patients are limited [17,19,36]. The microbial investigation of some Chinese and Mexican GCT samples showed that the most abundant microbes in the GCT samples were assigned to Proteobacteria, followed by oral-associated bacteria [17].…”

Section: Discussionmentioning

confidence: 99%

Microbial profiling identifies potential key drivers in gastric cancer patients

Wang

et al. 2021

Biotechnology & Biotechnological Equipment

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Gastric cancer (GC) is the fifth most commonly diagnosed cancer and the third leading cause of cancer-related death in the world. Microbiota is believed to be associated with GC. Growing evidences showed Helicobacter pylori played a key role in GC development. However, little was known about the microbiota in gastric juices and tissues in GC patients, and thus it was difficult to understand other potential microbial causation for GC. Here, we collected the gastric juice and surgically removed gastric tissues from GC patients to give insight into GC microbiota. Most microbes identified in the gastric samples were opportunistic pathogens or resident flora of the human microbiota. Further network analyses identified five opportunistic pathogens as keystone species. H. pylori is the direct cause of GC, but other opportunistic microbes might also function in GC development. The microbiota in the gastric juice and gastric tissue of the GC patients were complex, and some dominant opportunistic pathogens contributed to the GC development. This study introduces microbiota in gastric juice, gastric normal tissue and gastric cancer tissue of GC patients, and highlights the potential keystone microbes functioned during GC development.

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“…[24][25][26] This process can induce abnormal expression of some autophagy-related miRNAs, triggering regulatory disorders between miRNAs and target genes. 27 Although the mechanism between HP infection and COL4A1 abnormal expression in GC is not clear, it still indicated that COL4A1 might not only affect the malignancy of GC, but it also plays a biological role in promoting the progression of GC. In vitro experiments showed that downregulation of COL4A1 expression significantly inhibited the migration and invasion of GC cells from different growth patterns (Figure 9).…”

Section: Discussionmentioning

confidence: 99%

Identification of the Combinatorial Effect of miRNA Family Regulatory Network in Different Growth Patterns of GC

Cheng

Zhuo

Wang

et al. 2020

Molecular Therapy - Oncolytics

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According to the growth pattern, gastric cancer (GC) could be classified into expanding-type GC and infiltrative-type GC (Ming's classification). The growth pattern of GC is often related to the malignant degree, invasion, metastasis, and other pathological characteristics of tumors. MicroRNAs (miRNAs) play important roles in modulating gene expression during the GC development. In this study, miR-29s were significantly correlated with the gastric carcinogenesis and Ming's classification. Biological function of miR-29s is most closely related to the pathway of extracellular matrix (ECM)-receptor interaction. ECM structural assembly, cell movement, and cell adhesion are the main functional categories of target genes in this pathway. Among these targets, the COL4A1 gene ranked at the top in the association analysis of combined miR-29s biological function and GC subtype, and miR-29s inhibited its translation by binding to the 3 0 UTR region. Infiltrative-type GC cells secrete a higher level of COL4A1 protein than do expanding-type GC cells. The expression of COL4A1 in GC is correlated with clinicopathological features. Downregulation of COL4A1 expression significantly inhibited the migration and invasion of GC cells. High COL4A1 expression was correlated with poor prognosis in survival analysis. The miR-29s regulatory network may affect the development of growth patterns and pathological progress of GC by regulating the function of COL4A1.

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Current information on the association of Helicobacter pylori with autophagy and gastric cancer

Cited by 40 publications

References 66 publications

Effect of Astaxanthin on Activation of Autophagy and Inhibition of Apoptosis in Helicobacter pylori-Infected Gastric Epithelial Cell Line AGS

Effect of Astaxanthin on Activation of Autophagy and Inhibition of Apoptosis in Helicobacter pylori-Infected Gastric Epithelial Cell Line AGS

Microbial profiling identifies potential key drivers in gastric cancer patients

Identification of the Combinatorial Effect of miRNA Family Regulatory Network in Different Growth Patterns of GC

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