Full-Text Search:
Home|About CNKI|User Service|中文
Add to Favorite Get Latest Update

Effects of C23 in BMP2 induced EMT in gastric cancer cells

ZHANG Jianping;YANG Lijuan;ZHAO Huiying;YANG Yonggang;SHI Yinghua;YIN Shanshan;ZHANG Wenliang;Department of Geriatrics,the First Hospital of Shijiazhuang City;  
Objective In previous study,the epithelial to mesenchymal transition(EMT) has been identified to beinvolved in gastric cancer progression.Notably,nuclear protein C23 and bone morphogenetic protein-2(BMP2) have been linked into EMT.However,the specific mechanisms underlying BMP2 pathway-mediated EMT are not still unraveled.The paper investigated the biological role of C23 in BMP2-induced EMT in gastric cancer cells.Methods The study adopted immunohistochemistry and immunoblotting to determine the expression of C23 and BMP2 receptor Ⅱ(BMPR-Ⅱ) in various gastric cancer cell lines.Subsequently,gastric cancer cell lines were selected to be treated with si C23 and detected the changes of the EMT related indicators after C23 expression was blocked.Results Both C23 and BMPR-Ⅱ were aberrandy and constitutively expressed in gastric cancer cell lines.In vitro assay validated the increased expression of p-Erk1/2,p-Akt,vimentin,Ncadherin and MMP-2 in BMP2 stimulated MGC803 cells,which was in a dose dependent manner.By contrast,si-C23 treatment attenuated the BMP2 stimulated expression of p-Erk1/2,p-Akt,vimentin,N-cadherin and MMP-2.Also,the treatment of either si-C23 decreased the ability of migration and invasion of MGC803 cells.Conclusion C23 protein meditates bone morphogenetic protein 2 mediated EMT via up regulating of Erk1/2 and Akt in gastric cancer,which indicated both C23 and BMPR-Ⅱ pathway could be recommended as prospective targets or biomarkers to antagonize the progression of gastric cancer.
Download(CAJ format) Download(PDF format)
CAJViewer7.0 supports all the CNKI file formats; AdobeReader only supports the PDF format.
©CNKI All Rights Reserved