Activation of Aquaporin 5 by carcinogenic Helicobacter pylori infection promotes epithelial‐mesenchymal transition via the MEK/ERK pathway

Helicobacter ◽  
2021 ◽  
Author(s):  
Nianshuang Li ◽  
Xinbo Xu ◽  
Hui Yang ◽  
Huan Wang ◽  
Yaobin Ouyang ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Mesenchymal Transition ◽  
Helicobacter Pylori Infection ◽  
Erk Pathway ◽  
Aquaporin 5 ◽  
Mesenchymal Transition

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

Sa1872 Helicobacter pylori cag+ Strains Induce Epithelial-Mesenchymal Transition via Activation of P120

2013 ◽  
Vol 144 (5) ◽  
pp. S-324
Author(s):  
Lydia E. Wroblewski ◽  
M. Blanca Piazuelo ◽  
Pelayo Correa ◽  
Albert B. Reynolds ◽  
Richard M. Peek
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals Helicobacter pylori generates cells with cancer stem cell properties via epithelial–mesenchymal transition-like changes

Oncogene ◽  
2013 ◽  
Vol 33 (32) ◽  
pp. 4123-4131 ◽  
Author(s):  
E Bessède ◽  
C Staedel ◽  
L A Acuña Amador ◽  
P H Nguyen ◽  
L Chambonnier ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

Aquaporin-5 regulation of cell-cell adhesion proteins: an elusive "tail" story

2020 ◽  
Author(s):  
Frédéric H. Login ◽  
Johan Palmfeldt ◽  
Joleen Cheah ◽  
Soichiro Yamada ◽  
Lene N. Nejsum
Keyword(s):  
Cell Adhesion ◽  
Water Transport ◽  
Epithelial Mesenchymal Transition ◽  
Tail Domain ◽  
Aquaporin 5 ◽  
Mesenchymal Transition ◽  
Cancer Spread ◽  
Aqp5 Expression ◽  
Migration Capacity ◽  
Cell Cell

Aquaporins (AQPs) are water channels that facilitate transport of water across cellular membranes. AQPs are overexpressed in several cancers. Especially in breast cancer, AQP5 overexpression correlates with spread to lymph nodes and poor prognosis. Previously, we showed that AQP5 expression reduced cell-cell adhesion by reducing levels of adherens and tight junction proteins (e.g., ZO1, plakoglobin and β-catenin) at the actual junctions. Here, we show that when targeted to the plasma membrane, the AQP5 C-terminal tail domain regulated junctional proteins. Moreover, that AQP5 interacted with ZO1, plakoglobin, β-catenin and desmoglein-2, which were all reduced at junctions upon AQP5 overexpression. Thus, our data suggest that AQP5 mediates the effect on cell-cell adhesion via interactions with junctional protein independently of AQP5 mediated water transport. AQP5 overexpression in cancers may thus contribute to carcinogenesis and cancer spread by two independent mechanisms: reduced cell-cell adhesion, a characteristic of epithelial-mesenchymal transition, and increased cell migration capacity via water transport.

Antiflammin-1 Inhibits the TGF-β1-Induced Epithelial-Mesenchymal Transition in A549 Cells Through ERK Pathway

CHEST Journal ◽  
2016 ◽  
Vol 149 (4) ◽  
pp. A309 ◽  
Author(s):  
Wei Liu ◽  
Yang Li ◽  
Si-yuan Tang ◽  
Zi-Qiang Luo
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
A549 Cells ◽  
Erk Pathway ◽  
Mesenchymal Transition ◽  
Tgf Β1
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