scholarly journals Afadin Downregulation by Helicobacter pylori Induces Epithelial to Mesenchymal Transition in Gastric Cells

2018 ◽  
Vol 9 ◽  
Author(s):  
Miguel Sardinha Marques ◽  
Joana Melo ◽  
Bruno Cavadas ◽  
Nuno Mendes ◽  
Luísa Pereira ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Gastric Cells

Investigating Helicobacter pylori-related pyloric hypomotility; Functional, histological and molecular alterations

2021 ◽  
Author(s):  
Aya Aly Ashraf ◽  
Sarah Mahmoud Gamal ◽  
Hend Ashour ◽  
Basma Emad Aboulhoda ◽  
Laila Ahmed Rashed ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Smooth Muscle ◽  
Triple Therapy ◽  
Epithelial To Mesenchymal Transition ◽  
Ex Vivo ◽  
Vehicle Group ◽  
Mesenchymal Transition ◽  
H Pylori ◽  
Serum Ghrelin ◽  
E Cadherin

Multiple theories have been proposed describing the pathogenic mechanisms of Helicobacter pylori (H. pylori)-associated gastric motility disorders. We assessed ex-vivo pyloric activity in h.pylori infected rats, and tried to explore the associated ghrelin hormone alteration and pyloric fibrogenesis. In addition, miR-1 was assessed in pyloric tissue samples, being recently accused of having a role in smooth muscle dysfunction. Ninety adult male Wistar albino rats were assigned into 9 groups: 1)Control group, 2)Sterile broth (vehicle group), 3)amoxicillin control, 4) omeperazole control, 5)clarithromycin control, 6)triple therapy control, 7)H. pylori- group, 8)H. pylori-clarithromycin group, and 9)H.pylori-triple therapy group. Urease enzyme activity was applied as an indicator of H. pylori infection. Ex-vivo pyloric contractility was evaluated. Serum ghrelin was assessed, and histological tissue evaluation was performed. Besides, pyloric muscle miR-1 expression was measured. The immunological epithelial to mesenchymal transition (EMT) markers; transforming growth factor β (TGFβ), alpha-smooth muscle actin (α-SMA) and E-cadherin-3 were also evaluated. By H. pylori infection, a significant (P<0.001) reduced pyloric contractility index was recorded. The miR-1 expression was decreased (P<0.001) in the H. pylori-infected group, associated with reduced serum ghrelin, elevated TGFβ, and α-SMA levels and reduced E-cadherin levels. Decreased miR-1 and disturbed molecular pattern were improved by treatment. In conclusion: H. pylori infection was associated with reduced miR-1, epithelial to mesenchymal transition, and pyloric hypomotility. The miR-1 may be a target for further studies to assess its possible involvement in H.pylori associated pyloric dysfunction, which might help in management of human H. pylori manifestations and complications.

scholarly journals Infection with CagA+Helicobacter pylori induces epithelial to mesenchymal transition in human cholangiocytes

2020 ◽  
Author(s):  
Prissadee Thanaphongdecha ◽  
Shannon E. Karinshak ◽  
Wannaporn Ittiprasert ◽  
Victoria H. Mann ◽  
Yaovalux Chamgramol ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial To Mesenchymal Transition ◽  
Cellular Proliferation ◽  
Stem Cell Marker ◽  
Migration And Invasion ◽  
Cell Contact ◽  
Cell Of Origin ◽  
Mesenchymal Transition ◽  
H Pylori

AbstractRecent reports suggest that the East Asian liver fluke, Opisthorchis viverrini, infection with which is implicated in opisthorchiasis-associated cholangiocarcinoma, serves as a reservoir of Helicobacter pylori. The opisthorchiasis-affected cholangiocytes that line the intrahepatic biliary tract are considered to be the cell of origin of this malignancy. Here, we investigated interactions in vitro among human cholangiocytes, a CagA-positive strain of Helicobacter pylori, and the related bacillus, Helicobacter bilis. Exposure to increasing numbers of H. pylori at 0, 1, 10, 100 bacilli per cholangiocyte induced phenotypic changes including the profusion of thread-like filopodia and a loss of cell-cell contact, in a dose-dependent fashion. In parallel, following exposure to H. pylori, changes were evident in levels of mRNA expression of epithelial to mesenchymal transition (EMT)-encoding factors including snail, slug, vimentin, matrix metalloprotease, zinc finger E-box-binding homeobox, and the cancer stem cell marker CD44. Transcription levels encoding the cell adhesion marker CD24 decreased. Analysis to quantify cellular proliferation, migration and invasion in real time using the xCELLigence approach revealed that exposure to ≥10 H. pylori stimulated migration and invasion by the cholangiocytes through an extracellular matrix. In addition, 10 bacilli of CagA-positive H. pylori stimulated contact-independent colony establishment in soft agar. These findings support the hypothesis that infection with H. pylori contributes to the malignant transformation of the biliary epithelium.

scholarly journals Infection with Helicobacter pylori Induces Epithelial to Mesenchymal Transition in Human Cholangiocytes

Pathogens ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 971
Author(s):  
Prissadee Thanaphongdecha ◽  
Shannon E. Karinshak ◽  
Wannaporn Ittiprasert ◽  
Victoria H. Mann ◽  
Yaovalux Chamgramol ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial To Mesenchymal Transition ◽  
Cellular Proliferation ◽  
Stem Cell Marker ◽  
Migration And Invasion ◽  
Cell Contact ◽  
Cell Of Origin ◽  
Mesenchymal Transition ◽  
H Pylori

Recent reports suggest that the East Asian liver fluke infection, caused by Opisthorchis viverrini, which is implicated in opisthorchiasis-associated cholangiocarcinoma, serves as a reservoir of Helicobacter pylori. The opisthorchiasis-affected cholangiocytes that line the intrahepatic biliary tract are considered to be the cell of origin of this malignancy. Here, we investigated interactions in vitro among human cholangiocytes, Helicobacter pylori strain NCTC 11637, and the congeneric bacillus, Helicobacter bilis. Exposure to increasing numbers of H. pylori at 0, 1, 10, 100 bacilli per cholangiocyte of the H69 cell line induced phenotypic changes including the profusion of thread-like filopodia and a loss of cell-cell contact, in a dose-dependent fashion. In parallel, following exposure to H. pylori, changes were evident in levels of mRNA expression of epithelial to mesenchymal transition (EMT)-encoding factors including snail, slug, vimentin, matrix metalloprotease, zinc finger E-box-binding homeobox, and the cancer stem cell marker CD44. Analysis to quantify cellular proliferation, migration, and invasion in real-time by both H69 cholangiocytes and CC-LP-1 line of cholangiocarcinoma cells using the xCELLigence approach and Matrigel matrix revealed that exposure to ≥10 H. pylori bacilli per cell stimulated migration and invasion by the cholangiocytes. In addition, 10 bacilli of H. pylori stimulated contact-independent colony establishment in soft agar. These findings support the hypothesis that infection by H.pylori contributes to the malignant transformation of the biliary epithelium.

The role of DUBs in the post-translational control of cell migration

2019 ◽  
Vol 63 (5) ◽  
pp. 579-594 ◽  
Author(s):  
Guillem Lambies ◽  
Antonio García de Herreros ◽  
Víctor M. Díaz
Keyword(s):  
Cell Migration ◽  
Translational Control ◽  
Epithelial To Mesenchymal Transition ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Mesenchymal Transition ◽  
Tgfβ Receptors ◽  
Fundamental Process ◽  
Multistep Process

Abstract Cell migration is a multifactorial/multistep process that requires the concerted action of growth and transcriptional factors, motor proteins, extracellular matrix remodeling and proteases. In this review, we focus on the role of transcription factors modulating Epithelial-to-Mesenchymal Transition (EMT-TFs), a fundamental process supporting both physiological and pathological cell migration. These EMT-TFs (Snail1/2, Twist1/2 and Zeb1/2) are labile proteins which should be stabilized to initiate EMT and provide full migratory and invasive properties. We present here a family of enzymes, the deubiquitinases (DUBs) which have a crucial role in counteracting polyubiquitination and proteasomal degradation of EMT-TFs after their induction by TGFβ, inflammatory cytokines and hypoxia. We also describe the DUBs promoting the stabilization of Smads, TGFβ receptors and other key proteins involved in transduction pathways controlling EMT.

Roles of Helicobacter pylori in the Epithelial-Mesenchymal Transition of Gastric Cancer

2020 ◽  
Vol 04 (04) ◽  
Author(s):  
Shuai Ruan ◽  
Wenjie Huang ◽  
Fang Wen ◽  
Xiaona Lu ◽  
Su Ping Gu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition
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