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Helicobacter pylori Might Induce TGF-β1-Mediated EMT by Means of cagE.
- Source :
-
Helicobacter . Dec2015, Vol. 20 Issue 6, p438-448. 11p. - Publication Year :
- 2015
-
Abstract
- Background: Epithelial--mesenchymal transition (EMT), in which polarized epithelial cells have mesenchymal cell phenotypes, is thought to be a key process of invasion and metastasis of cancer. Transforming growth factor beta-1 (TGF-β1) is known to be carcinogenic and Helicobacter pylori is a predominant carcinogen of gastric cancer. Our study aimed to determine whether TGF-β1 or H. pylori infection enhances EMT process and cytotoxinassociated gene E (CagE) is associated with EMT. Materials and Methods: Human gastric cancer cell AGS and MKN45 were treated with recombinant TGF-β1 or H. pylori including cagE-negative (DcagE) mutant. Besides the assessment of EMT-related markers expression levels by means of RT-qPCR, Western blot, and immunofluorescence assay, the induction of in vitro EMT on gastric cancer cells (AGS and MKN cell lines) was confirmed by wound-healing assay and invasion assay. Results: When gastric cancer cells were treated with TGF-β1 or various strains of cagE-positive H. pylori, EMT-related marker altered significantly. However, the DcagE mutant did not. Wound-healing assay and invasion assay showed enhanced migration ability of the cells treated with cagE-positive H. pylori but not in DcagE mutant. Conclusions: EMT induction in gastric cancer cells by TGF-β1 was con- firmed. Only infection with cagE-positive H. pylori upregulated the TGF-β1-mediated EMT pathway and consequently promotes EMT. Therefore, H. pylori might induce TGF-β1-mediated EMT associated with the cagE. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10834389
- Volume :
- 20
- Issue :
- 6
- Database :
- Academic Search Index
- Journal :
- Helicobacter
- Publication Type :
- Academic Journal
- Accession number :
- 111348252
- Full Text :
- https://doi.org/10.1111/hel.12220