microRNA-637 promotes apoptosis and suppresses proliferation and autophagy in multiple myeloma cell lines via NUPR1

microRNA-637 通过 NUPR1 促进多发性骨髓瘤细胞系凋亡并抑制增殖和自噬

阅读:7
作者:Xuanxin Chen, Anmao Li, Qian Zhan, Zizi Jing, Yiyu Chen, Jianbin Chen

Abstract

Multiple myeloma (MM) is a heterogeneous disease with poor prognosis. Increasing evidence has revealed that microRNAs (miRNAs) are strongly associated with the pathogenesis and progression of MM. Here, we investigated the role of microRNA-637 (miR-637) in MM to identify potential therapeutic targets. We measured the expression of miR-637 in bone marrow samples of MM patients and MM cell lines by quantitative real-time PCR and western blot. The effect of miR-637 on proliferation and apoptosis of MM primary cells was also investigated. Analyses of four bioinformatics databases showed that miR-637 is associated with nuclear protein 1 (NUPR1) in MM cells, which was confirmed by luciferase reporter assay. We found that the overexpression of miR-637 suppressed the development of MM. miR-637 mimics increased the levels of Bax, cleaved caspase 3, and P62, and decreased the levels of Bcl2 and LC3. Additionally, luciferase reporter assays were performed to demonstrate that NUPR1 is the main target of miR-637 in MM cells. Overexpression of NUPR1 reversed the effects of miR-637 mimics in MM cells. Our results suggest that miR-637 inhibits cell proliferation and autophagy, and promotes apoptosis in MM cells by targeting NUPR1. Our findings also suggest that miR-637 may have potential as a novel molecular therapeutic target for MM 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。