ArticleMolecular and cellular biochemistry2011
Nuclear translocation of β-catenin correlates with CD44 upregulation in Helicobacter pylori-infected gastric carcinoma.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Precancerous pathways to gastric cancer: a review of experimental animal models recapitulating the correa cascade.Frontiers in cell and developmental biology · 2025Review
- Shigella dysenteriae infection activates proinflammatory response through β-catenin/NF-κB signaling pathway.PloS one · 2017Article
- The metastasis suppressor, NDRG1, inhibits "stemness" of colorectal cancer via down-regulation of nuclear β-catenin and CD44.Oncotarget · 2015Article
- Inhibition of β-catenin and STAT3 with a curcumin analog suppresses gastric carcinogenesis in vivo.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2015Article
- Myricetin induces apoptosis by inhibiting P21 activated kinase 1 (PAK1) signaling cascade in hepatocellular carcinoma.Molecular and cellular biochemistry · 2015Article
- Antral atrophy, intestinal metaplasia, and preneoplastic markers in Mexican children with Helicobacter pylori-positive and Helicobacter pylori-negative gastritis.Annals of diagnostic pathology · 2014Article
- Expression of APC, β-catenin and E-cadherin in Tunisian patients with gastric adenocarcinoma: clinical significance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- iNOS activation regulates β-catenin association with its partners in endothelial cells.PloS one · 2012Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with Helicobacter pylori CagA-positive strains is associated with gastric adenocarcinoma. CagA H. pylori activates the β-catenin signal by translocation into nucleus which promotes carcinogenesis. Deregulated accumulation of nuclear β-catenin enhances transcription of β-catenin target genes including CD44 and promotes malignant transformation. The aim of this study was to investigate whether nuclear translocation of β-catenin correlates with CD44 expression in CagA H. pylori-infected gastric carcinoma. To address these issues, we examined 140 gastric biopsy specimens by using immunohistochemical and immunofluorescence staining, Western blot, and mutational analysis of the exon 3 β-catenin gene. The nuclear localization of β-catenin was significantly (χ(2) = 21.175; P < 0.001) increased in advanced gastric carcinoma and also correlated (χ(2) = 22.857; P < 0.001) with the CagA H. pylori positive specimens. We also observed that tyrosine-phosphorylated β-catenin was significantly (χ(2) = 14.207; P < 0.001) increased in samples showing nuclear localization of β-catenin and also it correlated (χ(2) = 43.69; P < 0.03) with the CagA H. pylori positive specimens. Exon 3 β-catenin gene mutation was not detected in H. pylori-infected gastric carcinoma. CD44 up regulation was significantly associated with tyrosine-phosphorylated β-catenin (χ(2) = 22.5; P < 0.001), and this change was closely associated with nuclear translocation of β-catenin (χ(2) = 13.393; P < 0.001) in CagA H. pylori-infected gastric carcinoma. In conclusion, our data suggest that CagA H. pylori infection is responsible for the tyrosine phosphorylation of β-catenin and its nuclear translocation, which upregulates β-catenin target gene CD44 in gastric carcinoma.
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