Helicobacter pyloriCagA and IL-1βPromote the Epithelial-to-Mesenchymal Transition in a Nontransformed Epithelial Cell Model
Autor: | Ezequiel M. Fuentes-Pananá, Haruki Arévalo-Romero, Gabriela Vallejo-Flores, Isaura Meza |
---|---|
Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Article Subject MMP9 digestive system CDH1 03 medical and health sciences Downregulation and upregulation medicine CagA Epithelial–mesenchymal transition lcsh:RC799-869 Hepatology biology business.industry Gastroenterology Cancer Helicobacter pylori bacterial infections and mycoses medicine.disease biology.organism_classification digestive system diseases 030104 developmental biology Immunology biology.protein bacteria lcsh:Diseases of the digestive system. Gastroenterology Gastritis medicine.symptom business Research Article |
Zdroj: | Gastroenterology Research and Practice Gastroenterology Research and Practice, Vol 2016 (2016) |
ISSN: | 1687-630X 1687-6121 |
DOI: | 10.1155/2016/4969163 |
Popis: | Gastric cancer is the third cause of cancer death worldwide and infection byHelicobacter pylori(H. pylori) is considered the most important risk factor, mainly by the activity of its virulence factor CagA.H. pylori/CagA-induced chronic inflammation triggers a series of gastric lesions of increased severity, starting with gastritis and ending with cancer. IL-1βhas been associated with tumor development and invasiveness in different types of cancer, including gastric cancer. Currently, it is not clear if there is an association between CagA and IL-1βat a cellular level. In this study, we analyzed the effects of IL-1βand CagA on MCF-10A nontransformed cells. We found evidence that both CagA and IL-1βtrigger the initiation of the epithelial-to-mesenchymal transition characterized byβ-catenin nuclear translocation, increased expression ofSnail1andZEB1, downregulation ofCDH1, and morphological changes during MCF-10A acini formation. However, only CagA induced MMP9 activity and cell invasion. Our data support that IL-1βand CagA target theβ-catenin pathway, with CagA leading to acquisition of a stage related to aggressive tumors. |
Databáze: | OpenAIRE |
Externí odkaz: |