Circular RNA circ_0084927 regulates proliferation, apoptosis, and invasion of breast cancer cells via miR-142-3p/ERC1 pathway

环状RNA circ_0084927通过miR-142-3p/ERC1通路调控乳腺癌细胞增殖、凋亡和侵袭

阅读:7
作者:Guohua Gong, Jikai She, Danni Fu, Dong Zhen, Bin Zhang

Conclusion

Circ_0084927 can promote the progression of BC by regulating the miR-142-3p/ERC1 axis.

Methods

The levels of circ_0084927, miR-142-3p, and ELKS/RAB6-interacting/CAST family member-1 (ERC1) mRNA in the BC tissues and cells were detected by qRT-PCR. CCK8, colony formation, Transwell, and flow cytometry assays were performed to examine the cell proliferation, colony formation, cell invasion, and apoptosis, respectively, in the BC cells with regulated expressions of circ_0084927, miR-142-3p, and ERC1. RNase R treatment was employed to verify the circular structure of circ_0084927. Nucleocytoplasmic separation experiment, bioinformatics analysis, dual-luciferase reporter assay, and RNA immunoprecipitation were performed to investigate the ceRNA mechanism of circ_0084927.

Objective

We aimed to investigate the mechanism of circular RNA circ_0084927 in the progression of breast cancer (BC).

Results

High levels of circ_0084927 and ERC1 and low levels of miR-142-3p were detected in the BC tissues and cells. Knockdown of circ_0084927 promoted apoptosis and inhibited proliferation, colony formation, and invasion of BC cells (all P<0.05), whereas overexpression of circ_0084927 in the BC cells achieved the opposite effects. miR-142-3p is the target of circ_0084927. Overexpression of miR-142-3p could inhibit BC cell proliferation, colony formation, and cell invasion and induce apoptosis of the BC cells (all P<0.05), and the effects of miR-142-3p knockout on the BC cells could be reversed by silencing circ_0084927. miR-142-3p could target ERC1. Both ERC1 silencing and circ_0084927 knockout in the BC cells could achieve the tumor-suppressing effect, and this effect could be more remarkable under simultaneous ERC1 silencing and circ_0084927 knockout (all P<0.05).

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。