microRNA-203 suppresses invasion of gastric cancer cells by targeting ERK1/2/Slug/ E-cadherin signaling

2017 ◽  
Vol 19 (1) ◽  
pp. 11-20 ◽  
Author(s):  
Peng Gao ◽  
Shijie Wang ◽  
Fuchun Jing ◽  
Jiang Zhan ◽  
Yunhui Wang
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
E Cadherin

scholarly journals Helicobacter pyloriinduces promoter methylation of E-cadherin via interleukin-1β activation of nitric oxide production in gastric cancer cells

Cancer ◽  
2012 ◽  
Vol 118 (20) ◽  
pp. 4969-4980 ◽  
Author(s):  
Fung-Yu Huang ◽  
Annie On-On Chan ◽  
Asif Rashid ◽  
Danny Ka-Ho Wong ◽  
Chi-Hin Cho ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Cancer ◽  
Cancer Cells ◽  
Promoter Methylation ◽  
Interleukin 1Β ◽  
Nitric Oxide Production ◽  
Gastric Cancer Cells ◽  
Oxide Production ◽  
E Cadherin

scholarly journals Effect of dexmedetomidine on miR-144-3p expression and epithelial mesenchymal transition in gastric cancer cells

2021 ◽  
Vol 20 (11) ◽  
pp. 2249-2253
Author(s):  
Zong Chen ◽  
Yong Ding ◽  
Ying Zeng ◽  
Zhifeng Chen ◽  
Xueping Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Control Group ◽  
Gastric Cancer Cells ◽  
Rat Cardiomyocytes ◽  
Mesenchymal Transition ◽  
Geo Database ◽  
E Cadherin

Purpose: To investigate the effect of dexmedetomidine (DEX) on epithelial mesenchymal transition (EMT) in gastric cancer cells, and the role of microRNA-144-3p (miR-144-3p) in the process.Methods: The effect of DEX on miRNA expression profile was analyzed using GEO database(https://www.ncbi.nlm.nih.gov/gds/). Human gastric cancer cells were cultured in vitro, and one group of cells was treated with saline for 48 h (control group). Cells treated with DEX at doses of 0.01, 0.1 and 1.0 μmol/L for 48 h were marked as low-, medium- and high-DEX concentration groups. The mRNA expression levels of miR-144-3p, ZEB1, E-cadherin and vimentin were determined using real-time quantitative polymerase chain reaction (RT-PCR), while the protein expressions of ZEB1, E-cadherin and vimentin were assayed with Western blotting. Cell proliferation was determined with CCK-8 assay, while metastasis was measured using Transwell assay.Results: The GEO database demonstrated that the expression of miR-144-3p in rat cardiomyocytes was significantly decreased after DEX treatment (p < 0.05). The expression of miR-144-3p was decreased in all groups, when compared to the control group, but the expressions of ZEB1 and vimentin were increased, while that of E-cadherin was down-regulated (p < 0.05). Cell proliferation in the high-DEX concentration group was decreased (p < 0.05). The degrees of cell invasion and migration were increased in the medium- and high-DEX concentration groups (p < 0.05).Conclusion: DEX promotes the metastasis of gastric cancer cells by regulation of epithelialmesenchymal transition (EMT) and the expression of miR-144-3p. This finding provides a new insight into the treatment of gastric cancer.

scholarly journals The NMD mRNA surveillance pathway downregulates aberrant E-cadherin transcripts in gastric cancer cells and in CDH1 mutation carriers

Oncogene ◽  
2008 ◽  
Vol 27 (30) ◽  
pp. 4255-4260 ◽  
Author(s):  
R Karam ◽  
J Carvalho ◽  
I Bruno ◽  
C Graziadio ◽  
J Senz ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Mutation Carriers ◽  
Mrna Surveillance ◽  
Cdh1 Mutation ◽  
E Cadherin

scholarly journals Yes-Associated Protein Is Required for ZO-1-Mediated Tight-Junction Integrity and Cell Migration in E-Cadherin-Restored AGS Gastric Cancer Cells

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1264
Author(s):  
Seon-Young Kim ◽  
Song-Yi Park ◽  
Hwan-Seok Jang ◽  
Yong-Doo Park ◽  
Sun-Ho Kee
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Ectopic Expression ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
Migration Of Cells ◽  
E Cadherin

Yes-associated protein (YAP) regulates numerous cellular homeostasis processes and malignant transformation. We found that YAP influences ZO-1-mediated cell migration using E-cadherin-restored EC96 cells derived from gastric malignant AGS cells. Ectopic expression of E-cadherin enhanced straightforward migration of cells, in comparison to the meandering movement of parental AGS cells. In EC96 cells, YAP and ZO-1 expression increased but nuclear YAP levels and activity were reduced. Nuclear factor-κB (NF-κB) mediated the increase in ZO-1 expression, possibly stabilizing cytoplasmic YAP post-translationally. Downregulation of YAP expression using siYAP RNA or stable knock-down inhibited straightforward cell migration by fragmenting ZO-1 containing tight junctions (TJs) but not adherens junctions, implying involvement of YAP in ZO-1-mediated cell migration. The association of YAP with ZO-1 was mediated by angiomotin (AMOT) because downregulation of AMOT dissociated YAP from ZO-1 and reduced cell migration. E-cadherin restoration in malignant cancer cells induced NF-κB signaling to enhance ZO-1 expression and subsequently stabilize YAP. At high expression levels, YAP associates with ZO-1 via AMOT at TJs, influencing ZO-1-mediated cell migration and maintaining TJ integrity.

scholarly journals E-cadherin-defective gastric cancer cells depend on Laminin to survive and invade

2015 ◽  
Vol 24 (20) ◽  
pp. 5891-5900 ◽  
Author(s):  
Joana Caldeira ◽  
Joana Figueiredo ◽  
Catarina Brás-Pereira ◽  
Patrícia Carneiro ◽  
Ana M. Moreira ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
E Cadherin
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