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
Abstract：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 aberrantly and constitutively expressed in gastric cancer cell lines.In vitro assay validated the increased expression of p-Erk1/2, p-Akt, vimentin,N-cadherin 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.
Keywords：Nuclear protein C23Bone morphogenetic protein 2Epithelial mesenchymal transitionGastric cancer
Publication Date：2017-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：4( 713-716 )