lncRNAs combine and crosstalk with NSPc1 in ATRA-induced differentiation of U87 glioma cells

在 ATRA 诱导的 U87 胶质瘤细胞分化中,lncRNA 与 NSPc1 结合并串扰

阅读:5
作者:Zhikong Liang, Yuliang Wang, Hui Li, Yi Sun, Yanhua Gong

Abstract

Nervous system polycomb 1 (NSPc1) is a member of the polycomb group (PcG) family of proteins and has been demonstrated to maintain the differentiation and pluripotency of stem cells. Long non-coding RNAs (lncRNAs) have been demonstrated to be involved in the control of pluripotency and differentiation in embryonic and pluripotent cells. In the present study, the expression levels of NSPc1 were associated with the malignant potential of various glioma cell lines. Additionally, lncRNAs were differentially expressed in glioblastoma cell lines. Following induced differentiation of U87 glioblastoma cells with all-trans retinoic acid, the expression levels of NSPc1 decreased initially, reaching its lowest point on day 6, but then subsequently increased until day 10. The expression of lncRNA candidates decreased in the cell differentiation stage. Additionally, the expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), sex-determining region of the Y chromosome-box 2 overlapping transcript (SOX2OT) and antisense non-coding RNA in the INK4 locus (ANRIL) was significantly altered relative to the expression levels of NSPc1. RNA immunoprecipitation (RIP) assays demonstrated that MALAT1, SOX2OT and ANRIL bind to NSPc1 in U87 glioblastoma cells and the enrichment of ANRIL in anti-NSPc1 antibody group was associated with the expression levels of NSPc1 during U87 cell differentiation. Small interfering RNA mediated downregulation of NSPc1 expression with MALAT1, SOX2OT and ANRIL, inhibited the proliferation, and promoted apoptosis in U87 cells. The results of the present study demonstrate that MALAT1, SOX2OT and ANRIL combine and crosstalk with NSPc1 in U87 cells to affect proliferation and apoptosis.

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。