Role of linc00174/miR-138-5p (miR-150-5p)/FOSL2 Feedback Loop on Regulating the Blood-Tumor Barrier Permeability.
FOSL2
blood-tumor barrier
linc00174
miR-138-5p
miR-150-5p
Journal
Molecular therapy. Nucleic acids
ISSN: 2162-2531
Titre abrégé: Mol Ther Nucleic Acids
Pays: United States
ID NLM: 101581621
Informations de publication
Date de publication:
06 Dec 2019
06 Dec 2019
Historique:
received:
14
04
2019
revised:
27
09
2019
accepted:
26
10
2019
pubmed:
4
12
2019
medline:
4
12
2019
entrez:
3
12
2019
Statut:
ppublish
Résumé
The blood-tumor barrier (BTB) limits the transport of chemotherapeutic drugs to brain tumor tissues and impacts the treatment of glioma. Long non-coding RNAs play critical roles in various biological processes of tumors; however, the function of these in BTB permeability is still unclear. In this study, we have identified that long intergenic non-protein coding RNA 174 (linc00174) was upregulated in glioma endothelial cells (GECs) from glioma tissues. Additionally, linc00174 was also upregulated in GECs from the BTB model in vitro. Knock down of linc00174 increased BTB permeability and reduced the expression of the tight junction-related proteins ZO-1, occludin, and claudin-5. Both bioinformatics data and results of luciferase reporter assays demonstrated that linc00174 regulated BTB permeability by binding to miR-138-5p and miR-150-5p. Furthermore, knock down of linc00174 inhibited FOSL2 expression via upregulating miR-138-5p and miR-150-5p. FOSL2 interacted with the promoter regions and upregulated the promoter activity of ZO-1, occludin, claudin-5, and linc00174 in GECs. In conclusion, the present study demonstrated that the linc00174/miR-138-5p (miR-150-5p)/FOSL2 feedback loop played an essential role in regulating BTB permeability.
Identifiants
pubmed: 31791014
pii: S2162-2531(19)30341-5
doi: 10.1016/j.omtn.2019.10.031
pmc: PMC6906710
pii:
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1072-1090Informations de copyright
Copyright © 2019. Published by Elsevier Inc.
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