Hsa_circ_0005273 acts as a sponge of miR-509-3p to promote the malignant behaviors of breast cancer by regulating HMMR expression

Hsa_circ_0005273作为miR-509-3p的海绵,通过调控HMMR的表达促进乳腺癌的恶性行为

阅读:9
作者:Yong Peng, Jianhua Cui, Kaiwen Ma, Xi Zhong

Background

Breast cancer (BC) is a common malignant tumor that threatens the health of women worldwide. Hsa_circ_0005273 has been identified as a carcinogenic factor in some solid tumors, including BC. However, the molecular mechanism of circ_0005273 in BC is poorly defined.

Conclusion

Circ_0005273 knockdown might repress BC cell malignant behaviors by regulating the miR-509-3p/HMMR axis, which might provide a potential therapeutic target for BC.

Methods

The expression of circ_0005273, miR-509-3p, and hyaluronan-mediated motility receptor (HMMR) mRNA in BC was detected by quantitative real-time polymerase chain reaction. Cell proliferation, migration, invasion, and apoptosis were detected by 5-ethynyl-2'-deoxyuridine, transwell, and flow cytometry assays. The glycolysis level was detected via specific kits. Western blot was used to detect protein expression. Binding between miR-509-3p and circ_0005273 or HMMR was also verified by dual-luciferase reporter, RNA pull-down, and RNA immunoprecipitation assays. Xenograft tumor model was used to detect tumor changes in mice, and immunohistochemistry assay was employed to detect Ki-67 abundance.

Results

Circ_0005273 was increased in BC tissues and cells. Circ_0005273 knockdown might inhibit BC cell proliferation, migration, invasion, glutamine metabolism, and induce apoptosis. Circ_0005273 was a miR-509-3p, and the repression role of circ_0005273 absence on BC cell development was weakened by miR-509-3p inhibitor or HMMR overexpression. Circ_0005273 up-regulated the expression of HMMR by sponging miR-509-3p. Additionally, circ_0005273 silencing might hinder tumor growth in vivo.

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。