RGD Reference Report - NF-κB/miR-223-3p/ARID1A axis is involved in Helicobacter pylori CagA-induced gastric carcinogenesis and progression. - Rat Genome Database

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NF-κB/miR-223-3p/ARID1A axis is involved in Helicobacter pylori CagA-induced gastric carcinogenesis and progression.

Authors: Yang, Fenghua  Xu, Yugang  Liu, Chao  Ma, Cunying  Zou, Shuiyan  Xu, Xia  Jia, Jihui  Liu, Zhifang 
Citation: Yang F, etal., Cell Death Dis. 2018 Jan 9;9(1):12. doi: 10.1038/s41419-017-0020-9.
RGD ID: 126781705
Pubmed: PMID:29317648   (View Abstract at PubMed)
PMCID: PMC5849037   (View Article at PubMed Central)
DOI: DOI:10.1038/s41419-017-0020-9   (Journal Full-text)

Infection with Helicobacter pylori (H. pylori) and the resulting gastric inflammation is regarded as the strongest risk factor for gastric carcinogenesis and progression. NF-κB plays an important role in linking H. pylori-mediated inflammation to cancer. However, the underlying mechanisms are poorly understood. In this study, we find that H. pylori infection induces miR-223-3p expression in H. pylori CagA-dependent manner. NF-κB stimulates miR-223-3p expression via directly binding to the promoter of miR-223-3p and is required for H. pylori CagA-mediated upregulation of miR-223-3p. miR-223-3p promotes the proliferation and migration of gastric cancer cells by directly targeting ARID1A and decreasing its expression. Furthermore, miR-223-3p/ARID1A axis is involved in CagA-induced cell proliferation and migration. In the clinical setting, the level of miR-223-3p is upregulated, while ARID1A is downregulated significantly in human gastric cancer tissues compared with the corresponding noncancerous tissues. The expression level of miR-223-3p is significantly higher in H. pylori-positive gastric cancer tissues than that in H. pylori-negative tissues. Moreover, a negative correlation between miR-223-3p and ARID1A expression is found in the gastric cancer tissues. Taken together, our findings suggested NF-κB/miR-223-3p/ARID1A axis may link the process of H. pylori-induced chronic inflammation to gastric cancer, thereby providing a new insight into the mechanism underlying H. pylori-associated gastric diseases.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ARID1AHumanstomach cancer  IEP mRNA:decreased expression:stomach (human)RGD 
Arid1aRatstomach cancer  ISOARID1A (Homo sapiens)mRNA:decreased expression:stomach (human)RGD 
Arid1aMousestomach cancer  ISOARID1A (Homo sapiens)mRNA:decreased expression:stomach (human)RGD 
MIR223Humanstomach cancer  IEP associated with Helicobacter Infections and mRNA:increased expression:stomach (human)RGD 
Mir223Mousestomach cancer  ISOMIR223 (Homo sapiens)associated with Helicobacter Infections and mRNA:increased expression:stomach (human)RGD 
Mir223Ratstomach cancer  ISOMIR223 (Homo sapiens)associated with Helicobacter Infections and mRNA:increased expression:stomach (human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Arid1a  (AT-rich interaction domain 1A)
Mir223  (microRNA 223)

Genes (Mus musculus)
Arid1a  (AT-rich interaction domain 1A)
Mir223  (microRNA 223)

Genes (Homo sapiens)
ARID1A  (AT-rich interaction domain 1A)
MIR223  (microRNA 223)


Additional Information