Helicobacter pylori Might Induce TGF‐β1‐Mediated EMT by Means of cagE. Issue 6 (3rd March 2015)
- Record Type:
- Journal Article
- Title:
- Helicobacter pylori Might Induce TGF‐β1‐Mediated EMT by Means of cagE. Issue 6 (3rd March 2015)
- Main Title:
- Helicobacter pylori Might Induce TGF‐β1‐Mediated EMT by Means of cagE
- Authors:
- Chang, Hyun
Kim, Nayoung
Park, Ji Hyun
Nam, Ryoung Hee
Choi, Yoon Jeong
Park, Seon Mee
Choi, Yoon Jin
Yoon, Hyuk
Shin, Cheol Min
Lee, Dong Ho - Abstract:
- 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 cytotoxin‐associated 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 (Δ cagE ) 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 Δ cagE 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 Δ cagE mutant. Conclusions: EMT induction in gastric cancer cells by TGF‐β1 was confirmed. 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‐mediatedAbstract: 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 cytotoxin‐associated 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 (Δ cagE ) 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 Δ cagE 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 Δ cagE mutant. Conclusions: EMT induction in gastric cancer cells by TGF‐β1 was confirmed. 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 . … (more)
- Is Part Of:
- Helicobacter. Volume 20:Issue 6(2015:Dec.)
- Journal:
- Helicobacter
- Issue:
- Volume 20:Issue 6(2015:Dec.)
- Issue Display:
- Volume 20, Issue 6 (2015)
- Year:
- 2015
- Volume:
- 20
- Issue:
- 6
- Issue Sort Value:
- 2015-0020-0006-0000
- Page Start:
- 438
- Page End:
- 448
- Publication Date:
- 2015-03-03
- Subjects:
- EMT -- Gastric cancer -- H. pylori -- TGF‐β1 -- cagE
Helicobacter -- Periodicals
Helicobacter infections -- Periodicals
Stomach -- Diseases -- Periodicals
616.3301405 - Journal URLs:
- http://firstsearch.oclc.org ↗
http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1523-5378 ↗
http://www.blackwell-synergy.com/member/institutions/issuelist.asp?journal=hel ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/hel.12220 ↗
- Languages:
- English
- ISSNs:
- 1083-4389
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4285.102500
British Library DSC - BLDSS-3PM
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- 1707.xml