CircTHBS1 facilitates the progression of interstitial cystitis depending on the regulation of miR-139-5p/MFN2 axis

CircTHBS1 通过调节 miR-139-5p/MFN2 轴促进间质性膀胱炎的进展

阅读:5
作者:Chen Jiang, Ming Xu, Jin Zhu, Dongrong Yang, Boxin Xue

Abstract

Circular RNA (circRNA) have been found to play an important role in the progression of many diseases, including interstitial cystitis (IC). However, the role of circTHBS1 in IC progression is still unclear. Exploring the role and potential molecular mechanism of circTHBS1 in the development of IC. The enzyme-linked immunosorbent assay was used to assess the levels of inflammatory cytokines. The expression levels of circTHBS1, microRNA (miR)-139-5p, and mitofusin 2 (MFN2) were evaluated using quantitative real-time PCR. Cell proliferation and migration were determined using MTT assay, Edu staining, and transwell assay. The protein levels of epithelial-mesenchymal transition (EMT) markers and MFN2 were examined using western blot analysis. The relationship between miR-139-5p and circTHBS1 or MFN2 was confirmed using the dual-luciferase reporter assay and RIP assay. CircTHBS1 was highly repressed in IC tissues and cells, and its expression was positively correlated with the inflammatory response of IC patients. CircTHBS1 could promote the proliferation, migration, EMT process, and inflammation of IC cells, while its knockdown had an opposite effect. CircTHBS1 could serve as a sponge of miR-139-5p, and miR-139-5p could participate in the regulation of circTHBS1 on IC cell progression. In addition, miR-139-5p could target MFN2, and it could inhibit the progression of IC cells by targeting MFN2. Furthermore, circTHBS1 sponged miR-139-5p to positively regulate MFN2. CircTHBS1 promoted IC cell proliferation, migration, EMT process, and inflammation by regulating the miR-139-5p/MFN2 axis indicating that circTHBS1 might be a potential target for IC treatment.

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。