| Literature DB >> 32713259 |
Xiaobai Liu1,2,3, Peiqi Wu4,5,6, Rui Su4,5,6, Yixue Xue4,5,6, Chunqing Yang1,2,3, Di Wang1,2,3, Xuelei Ruan4,5,6, Jian Zheng1,2,3, Yang Yang1,2,3, Zhen Li1,2,3, Yunhui Liu1,2,3.
Abstract
Blood-tumour barrier (BTB) has been known to significantly attenuate the efficacy of chemotherapy for glioma. In this report, we identified that insulin-like grown factor 2 mRNA-binding protein 2 (IGF2BP2) was over-expressed in glioma microvessel and glioma endothelial cells (GECs). Knockdown of IGF2BP2 decreased the expression of lncRNA FBXL19-AS1 and tight junction-related proteins, thereby promoting BTB permeability. FBXL19-AS1 was over-expressed and more enriched in the cytoplasm of GECs. In addition, FBXL19-AS1 could bind to 3'-UTR of ZNF765 mRNA and down-regulate ZNF765 mRNA expression through STAU1-mediated mRNA decay (SMD). The low expression of ZNF765 was discovered in GECs and verified to increase BTB permeability by inhibiting the promoter activities of tight junction-related proteins. Meanwhile, ZNF765 also inhibited the transcriptional activity of IGF2BP2, thereby forming a feedback loop in regulating the BTB permeability. Single or combined application of silenced IGF2BP2 and FBXL19-AS1 improved the delivery and antitumor efficiency of doxorubicin (DOX). In general, our study revealed the regulation mechanism of IGF2BP2/FBXL19-AS1/ZNF765 axis on BTB permeability, which may provide valuable insight into treatment strategy for glioma.Entities:
Keywords: FBXL19-AS1; IGF2BP2; blood-tumour barrier; stau1-mediated decay
Year: 2020 PMID： 32713259 PMCID： PMC7714532 DOI： 10.1080/15476286.2020.1795583
Source DB: PubMed Journal: RNA Biol ISSN： 1547-6286 Impact factor: 4.652