NF-κB/miR-18a-3p and miR-4286/BZRAP1 axis may mediate carcinogenesis in Helicobacter pylori―Associated gastric cancer

Tsai, Chi‐Cheng; Chen, Taiyu; Tsai, Kuen-Jang; Lin, Ming‐Wei; Hsu, Chia‐Yi; Wu, Deng‐Chyang; Tsai, Eing‐Mei; Hsieh, Tsung‐Hua

doi:10.1016/j.biopha.2020.110869

Cited by 28 publications

(25 citation statements)

References 29 publications

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“…For example, H. pylori infection enhances expression of NLRP3, an important inflammasome component, by decreasing miR-22 levels to trigger uncontrolled proliferation of gastric epithelial cells [57]. Tsai and colleagues found that miR-18a-3p and miR-4286 were significantly upregulated in H. pylori-associated GC [58]. Furthermore, overexpression of miR-18a-3p and miR-4286 promoted cancer cell proliferation and motility by targeting BZRAP1.…”

Section: Exosomal Ncrnas and Helicobacter Pylori (H Pylori)mentioning

confidence: 99%

Exosome-derived noncoding RNAs in gastric cancer: functions and clinical applications

et al. 2021

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Exosomes are a subpopulation of the tumour microenvironment (TME) that transmit various biological molecules to promote intercellular communication. Exosomes are derived from nearly all types of cells and exist in all body fluids. Noncoding RNAs (ncRNAs) are among the most abundant contents in exosomes, and some ncRNAs with biological functions are specifically packaged into exosomes. Recent studies have revealed that exosome-derived ncRNAs play crucial roles in the tumorigenesis, progression and drug resistance of gastric cancer (GC). In addition, regulating the expression levels of exosomal ncRNAs can promote or suppress GC progression. Moreover, the membrane structures of exosomes protect ncRNAs from degradation by enzymes and other chemical substances, significantly increasing the stability of exosomal ncRNAs. Specific hallmarks within exosomes that can be used for exosome identification, and specific contents can be used to determine their origin. Therefore, exosomal ncRNAs are suitable for use as diagnostic and prognostic biomarkers or therapeutic targets. Regulating the biogenesis of exosomes and the expression levels of exosomal ncRNAs may represent a new way to block or eradicate GC. In this review, we summarized the origins and characteristics of exosomes and analysed the association between exosomal ncRNAs and GC development.

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Section: Exosomal Ncrnas and Helicobacter Pylori (H Pylori)mentioning

confidence: 99%

Exosome-derived noncoding RNAs in gastric cancer: functions and clinical applications

et al. 2021

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“…Several other cellular factors, which contribute to the progression of gastric carcinoma through modulating the NF-κB signaling have been described and include Cullin 4A [ 64 ], TNF [ 65 ], stomach-specific protein gastrokine 1 (GKN1) [ 66 ], interleukin 17A [ 67 ], IL-1β polymorphisms [ 68 ], cytoskeleton protein radixin [ 69 ], fibroblast growth factor-inducible 14 (Fn14) [ 70 ], inhibitor of growth 4 (ING4) [ 71 ], trefoil factor 1 (TFF1) [ 72 ], connective tissue growth factor (CTGF) [ 73 ], carcinoembryonic antigen-related cell adhesion molecule 19 (CEACAM19) [ 74 ], DNA repair protein (Ku) [ 75 ], stress protein metallothionein 2A (MT2A) [ 76 ], deacetylase sirtuin 1 (SIRT1) [ 77 ], oncogenes latent membrane protein 1 (LMP1) and LMP2A [ 78 ], microRNAs [ 79 , 80 , 81 , 82 ], or spermine oxidase [ 83 ].…”

Section: Dysregulation Of Nf-κb In Gastric Cancermentioning

confidence: 99%

NF-κB in Gastric Cancer Development and Therapy

et al. 2021

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Gastric cancer is considered one of the most common causes of cancer-related death worldwide and, thus, a major health problem. A variety of environmental factors including physical and chemical noxae, as well as pathogen infections could contribute to the development of gastric cancer. The transcription factor nuclear factor kappa B (NF-κB) and its dysregulation has a major impact on gastric carcinogenesis due to the regulation of cytokines/chemokines, growth factors, anti-apoptotic factors, cell cycle regulators, and metalloproteinases. Changes in NF-κB signaling are directed by genetic alterations in the transcription factors themselves, but also in NF-κB signaling molecules. NF-κB actively participates in the crosstalk of the cells in the tumor micromilieu with divergent effects on the heterogeneous tumor cell and immune cell populations. Thus, the benefits/consequences of therapeutic targeting of NF-κB have to be carefully evaluated. In this review, we address recent knowledge about the mechanisms and consequences of NF-κB dysregulation in gastric cancer development and therapy.

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“…Hp LPS can engage gastric mucosal TLR4 [33], and the Hp virulence factor CagA is a potent factor inducing nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and IκB kinases (IKKs) activation via transforming growth factor β-activated kinase 1 (TAK1), a key regulator of inflammation cascades [34]. TLR-4 has been demonstrated in chronic active gastritis [35], precancerous cells and cancerous gastric cells [36]. In our study, TLR-4 concentrations, but not LPS, were significantly higher in the culture medium of biopsies from active gastritis than in those from inactive ones.…”

Section: Discussionmentioning

confidence: 99%

Tissue transglutaminase is involved in the inflammatory processes of active chronic gastritis

Riezzo

Orlando

Clemente

et al. 2021

ARCH BIOL SCI BELGRA

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Since tissue transglutaminase-2 (TG2) can represent a marker of inflammation for some gastrointestinal (GI) diseases, we aimed to evaluate TG2 and inflammatory markers? mucosal content in gastric antrum biopsies to shed light on the histological and biochemical background of chronic gastritis inflammation. Fifty-one of 78 patients who underwent upper GI endoscopy (UGIE) for dyspeptic symptoms, had a gastric biopsy. The symptom profile was assessed by a GI symptom rating scale (GSRS) score. Thirtyfive patients (69%) showed chronic gastritis. TG2, interleukin-6 (IL)-6, IL-8, IL-10, tumor necrosis factor (TNF)-?, lipopolysaccharides (LPS) and toll-like receptor (TLR)-4 were evaluated in serum and the culture medium of gastric biopsies. TG2, IL-8, IL-10, TLR-4 and TNF-? were significantly higher in active chronic gastritis than in the inactive one and were linked to macrophage concentration. IL-6 was significantly lower in the active form of chronic gastritis than in the inactive one and negatively correlated with TG2. Lastly, IL- 10 significantly correlated with the macrophage score. TG2 can exert an active role in chronic gastritis pathogenesis by cooperating with different markers of inflammation. It seems that TG2 can represent a possible therapeutic target for modulating inflammation and disease progression.

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NF-κB/miR-18a-3p and miR-4286/BZRAP1 axis may mediate carcinogenesis in Helicobacter pylori―Associated gastric cancer

Cited by 28 publications

References 29 publications

Exosome-derived noncoding RNAs in gastric cancer: functions and clinical applications

Exosome-derived noncoding RNAs in gastric cancer: functions and clinical applications

NF-κB in Gastric Cancer Development and Therapy

Tissue transglutaminase is involved in the inflammatory processes of active chronic gastritis

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