E2F1-directed activation of nc886 mediates drug resistance in cervical cancer cells via regulation of major vault protein

E2F1 指导的 nc886 激活通过调节主要穹窿蛋白介导宫颈癌细胞的耐药性

阅读:4
作者:Jing-Hua Li, Ming Wang, Rui Zhang, Wan-Li Gao, Shi-Hui Meng, Xue-Lian Ma, Xiao-Hui Hou, Li-Min Feng

Abstract

Non-coding RNAs are critical regulators of tumor biology. nc886, a recently identified non-coding RNA, is overexpressed in some tumors, but undetected in others. However, the precise role of nc886 remains unclear in cervical cancers. In this study, we found that nc886, major vault protein (MVP), and E2F1 exhibited coordinate expression as they were silenced in normal tissues but overexpressed in cervical cancer tissues. We subsequently demonstrate that nc886 upregulation was a critical response to chemotherapy treatment of cervical cancer cells. Mechanistically, inhibition of nc886 increased chemosensitivity, induced apoptosis, and suppressed the protein expression of MVP, a critical regulator of drug resistance. Furthermore, we identify E2F1 as a key transcription regulator of nc886 that directly interacts and modulates promoter activity. Taken together, we demonstrate that E2F1 sufficiently promotes nc886 transcription and in turn MVP expression to drive drug resistance in cervical cancer cells.

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。