Correlation of OGR1 with proliferation and apoptosis of breast cancer cells

OGR1与乳腺癌细胞增殖及凋亡的相关性

阅读:8
作者:Jianguo Zhang, Lei Che, Wenkai Sun, Jian Shang, Min Hao, Mengzi Tian

Abstract

Effects of ovarian cancer G-protein-coupled receptor 1 (OGR1) protein on proliferation and apoptosis of breast cancer cells, as well as its molecular mechanism were investigated. The MCF-7 cell line highly expressed OGR1 was constructed by transient transfection of eukaryotic expression vector using breast cancer cells. At the same time, cells were transfected with empty vector as controls. The effects of highly expressed OGR1 on cell growth, proliferation, apoptosis and other abilities were identified. In addition, the effects of highly expressed OGR1 on serine-threonine kinase (AKT), p53 and other genes were studied. It was proved in apoptosis experiment that highly expressed OGR1 protein in breast cancer cells could effectively increase the proportion of apoptosis of cells. Cell proliferation experiment revealed that the growth and proliferation abilities of breast cancer cells with highly expressed OGR1 were inhibited to some extent, compared with those of breast cancer cells with low expression of OGR1. Results of western blotting showed that the gene and protein expression levels of p53 in breast cancer cells with highly expressed OGR1 were increased. There was no significant difference in protein expression of AKT between breast cancer cells with low expression of OGR1 and those with highly expressed OGR1. However, the protein content of phosphorylated-AKT (p-AKT) in breast cancer cells with highly expressed OGR1 was lower than that in breast cancer cells with low expression of OGR1. The proliferation and apoptosis of breast cancer cells are influenced by the changes of OGR1 expression, which are correlated with the gene expression levels of AKT and p53 to some extent, but the detailed molecular mechanism requires additional study.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。