癌症研究
基因敲除
染色质免疫沉淀
ATG5型
生物
自噬
弥漫性大B细胞淋巴瘤
下调和上调
小RNA
分子生物学
淋巴瘤
细胞培养
基因表达
细胞凋亡
基因
免疫学
发起人
遗传学
作者
Hua‐Zhen Xu,Xiao‐Jing Yu,Ziyuan Yang,Qingjie Song,Shijuan Cheng,Zhenzhen He,Liyun Dai
出处
期刊:Life Sciences
[Elsevier BV]
日期:2021-12-01
卷期号:286: 119932-119932
被引量:11
标识
DOI:10.1016/j.lfs.2021.119932
摘要
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.In this study, we aimed to explore the regulatory mechanism of ARRDC1-AS1 in DLBCL cells.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.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.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.
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