| Aim: To discuss the regulation of CDH4/R-Cadherin to epithelial-mesenchymaltransition (EMT) from gastric cancer, and its effect on the property of cancer stemcell.Methods: CDH4was cloned from the normal gastric epithelial tissue andconstructed its eukaryotic expression vector, picked out the overexpression CDH4cellline from gastric cancer BGC-823and the interference expression CDH4cell linefrom normal gastric epithelial through Lentiviral transfection technology. Theexpression of E-Cadherin, vemintin, twist mRNA and proteins from the stabletransfected cell line was dected and compared the differences with control group. Themigration ability was compared through wound healing assay and transwell cellsexperiment. MTT was used to depict the growing curve of transfected cells. Thetumorigenic ability was compared by single factor analysis of variance.Results:(1) In cell siCDH4-GES-1, the expression of E-Cadherin mRNA andproteins was decreased, and that of vemintin and twist were increased, while in cellpLV-CDH4-BGC-823, they were opposite.(2) The migration was reinforced in cellsiCDH4-GES-1, while opposite in cell pLV-CDH4-BGC-823.(3)The proliferationrate was increased and tumorigenic ability was reinforced in cell siCDH4-GES-1, thetumorigenic rate of siCDH4to pLKO.1-puro was9.53%±0.82%vs2.8%±0.52%,P<0.001. While it was opposite in cell pLV-CDH4-BGC-823, the tumorigenic rate ofpLV-CDH4to pLV-CS2.0was6.80%±0.37%vs17.50%±0.63%, P<0.05.Conclusion: CDH4/R-Cadherin as a key factor in decreasing the gastric epithelial cell EMT and acquiring the property of cancer stem cell, would inhibit the malignantbiological behavior of gastric cancer. Above all, CDH4/R-Cadherin probably becomepotential tumor inhibitory gene, and CDH4/R-Cadherin targeted therapy may providea new direction for tumor therapy. |
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