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.

Aim

In this study, we aimed to explore the regulatory mechanism of ARRDC1-AS1 in DLBCL cells.

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.

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.

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.

中文翻译：

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PAX5激活的lncRNA ARRDC1-AS1通过海绵miR-2355-5p调节ATG5加速DLBCL的自噬和进展

背景

弥漫性大 B 细胞淋巴瘤 (DLBCL) 具有很高的癌症相关死亡率。研究支持lncRNAs可以通过影响细胞自噬来调节癌症进展。发现 ARRDC1 反义 RNA 1 (ARRDC1-AS1) 在 GEPIA 的 DLBCL 组织中上调，但从未在 DLBCL 中检测到。

目标

本研究旨在探讨ARRDC1-AS1在DLBCL细胞中的调控机制。

主要方法

采用RT-qPCR检测DLBCL细胞中ARRDC1-AS1、microRNA-2355-5p（miR-2355-5p）和自噬相关基因5（ATG5）的表达。进行蛋白质印迹以检测蛋白质水平。DLBCL 细胞的恶性行为是通过功能测定来估计的。通过染色质免疫沉淀 (ChIP)、RNA pull-down、RNA 免疫沉淀 (RIP) 和荧光素酶报告基因检测检测分子相互作用。

结果

我们发现 ARRDC1-AS1 在 DLBCL 组织和细胞系中上调。ARRDC1-AS1 被转录因子 PAX5 激活。敲除 ARRDC1-AS1 可抑制 DLBCL 自噬以加剧增殖、抑制细胞凋亡并促进侵袭和迁移。此外，ARRDC1-AS1 吸附 miR-2355-5p 以上调 ATG5。

结论

目前的研究首先表明，PAX5 激活的 ARRDC1-AS1 通过海绵 miR-2355-5p 调节 ATG5 加速 DLBCL 的自噬和进展，揭示了 ARRDC1-AS1 在 DLBCL 中的新分子机制，并表明 ARRDC1-AS1 作为潜在靶点DLBCL。