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PAX5-activated lncRNA ARRDC1-AS1 accelerates the autophagy and progression of DLBCL through sponging miR-2355-5p to regulate ATG5.

Authors :
Xu H
Yu X
Yang Z
Song Q
Cheng S
He Z
Dai L
Source :
Life sciences [Life Sci] 2021 Dec 01; Vol. 286, pp. 119932. Date of Electronic Publication: 2021 Sep 06.
Publication Year :
2021

Abstract

Background: Diffuse large B-cell lymphoma (DLBCL) has high cancer-related mortality. Studies have supported that lncRNAs can regulate cancer progression by affecting autophagy of cells. ARRDC1 antisense RNA 1 (ARRDC1-AS1) was found to be upregulated in DLBCL tissues in GEPIA, but it has never been detected in DLBCL.<br />Aim: In this study, we aimed to explore the regulatory mechanism of ARRDC1-AS1 in DLBCL cells.<br />Main Methods: RT-qPCR was taken to measure the expression of ARRDC1-AS1, microRNA-2355-5p (miR-2355-5p) and autophagy-related gene 5 (ATG5) in DLBCL cells. Western blot was conducted to detect protein levels. The malignant behaviors of DLBCL cells were estimated through functional assays. The molecular interactions were detected by Chromatin immunoprecipitation (ChIP), RNA pull-down, RNA immunoprecipitation (RIP) and luciferase reporter assays.<br />Results: We found that ARRDC1-AS1 was upregulated in DLBCL tissues and cell lines. ARRDC1-AS1 was activated by transcription factor PAX5. Knockdown of ARRDC1-AS1 suppressed DLBCL autophagy to aggravate proliferation, repress apoptosis, and facilitate invasion and migration. Furthermore, ARRDC1-AS1 sponged miR-2355-5p to upregulate ATG5.<br />Conclusion: Present study first showed that PAX5-activated ARRDC1-AS1 accelerates the autophagy and progression of DLBCL via sponging miR-2355-5p to regulate ATG5, revealing a novel molecular mechanism of ARRDC1-AS1 in DLBCL and suggested ARRDC1-AS1 as a potential target in DLBCL.<br /> (Copyright © 2021 Elsevier Inc. All rights reserved.)

Details

Language :
English
ISSN :
1879-0631
Volume :
286
Database :
MEDLINE
Journal :
Life sciences
Publication Type :
Academic Journal
Accession number :
34499929
Full Text :
https://doi.org/10.1016/j.lfs.2021.119932