Long non-coding RNA CUDR promotes malignant phenotypes in pancreatic ductal adenocarcinoma via activating AKT and ERK signaling pathways

长链非编码RNA CUDR通过激活AKT和ERK信号通路促进胰腺导管腺癌的恶性表型

阅读:6
作者:Xing Liang, Meiyan Qi, Rui Wu, Anan Liu, Danlei Chen, Liang Tang, Jun Chen, Xiangui Hu, Wei Li, Lixing Zhan, Chenghao Shao

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, with a marked potential for invasion and metastasis. Emerging evidence has suggested that dysregulation of long non-coding RNAs (lncRNAs) is associated with the development of multiple types of cancer. However, the function of lncRNAs in PDAC is poorly known. In the present study, a microarray assay was used to screen for differently expressed lncRNAs in PDAC and it was identified that cancer upregulated drug resistance (CUDR) was upregulated in PDAC. CUDR increased PDAC cell proliferation, migration and invasion, inhibited apoptosis, and promoted drug resistance; it also regulated the PDAC cell epithelial-mesenchymal transition. The CUDR-induced PDAC malignant phenotypes is via the protein kinase B and extracellular-signal-regulated kinase signaling pathways. Downregulation of CUDR may be a novel therapeutic strategy to prevent PDAC development and drug resistance in the future.

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。