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CD5 阳性复发/难治性弥漫性大 B 细胞淋巴瘤中差异表达的 tRFs 及其潜在临床应用的生物信息学分析。

Differentially expressed tRFs in CD5 positive relapsed & refractory diffuse large B cell lymphoma and the bioinformatic analysis for their potential clinical use.

机构信息

Department of Hematology, Shandong Provincial Hospital Affiliated to Shandong University, No.324, Jingwu Road, Jinan, Shandong, 250021, People's Republic of China.

出版信息

Biol Direct. 2019 Nov 27;14(1):23. doi: 10.1186/s13062-019-0255-8.

Abstract

BACKGROUND

Patients diagnosed as diffuse large B cell lymphoma (DLBCL) with CD5 positive normally have a worse outcome and poorly respond to the regulatory treatment strategy.

RESULTS

We recently reported differently expressed tRFs and their potential target-genes of tRFs in patients with CD5+ R/R DLBCL. Differently expressed tRFs were detected by Illumina NextSeq instrument and the results were verified by quantitative real-time reverse transcription-PCR. tRF2Cancer database was searched to compared with the results. Further research was performed through bio-informatic analysis including gene ontology (GO) and pathway enrichment analyses, etc. A total of 308 tRFs were identified. Two sequences (AS-tDR-008946, AS-tDR-013492) were chosen for further investigated.

CONCLUSIONS

The results of Bioinformatics analysis revealed that the target genes including NEDD4L and UBA52 and several associated pathways including PI3K/AKT and MAPK/ERK might be involved in the development of CD5+ R/R DLBCL. Our preliminary study on the associated tRFs might provide a valuable measure to explore the pathogenesis and progression of CD5+ R/R DLBCL.

REVIEWERS

This article was reviewed by Zhen Qing Ye, Nagarajan Raju and Jin Zhuang Dou.

摘要

背景

CD5 阳性弥漫性大 B 细胞淋巴瘤(DLBCL)患者的预后通常较差,对调节治疗策略的反应不佳。

结果

我们最近报道了 CD5+R/R DLBCL 患者中差异表达的 tRFs 及其潜在的 tRFs 靶基因。通过 Illumina NextSeq 仪器检测差异表达的 tRFs,并通过定量实时逆转录-PCR 进行验证。在 tRF2Cancer 数据库中进行了比较。通过包括基因本体论(GO)和途径富集分析等生物信息学分析进一步研究。共鉴定出 308 个 tRFs。选择了两个序列(AS-tDR-008946、AS-tDR-013492)进行进一步研究。

结论

生物信息学分析结果表明,靶基因包括 NEDD4L 和 UBA52,以及几个相关途径,包括 PI3K/AKT 和 MAPK/ERK,可能参与了 CD5+R/R DLBCL 的发生发展。我们对相关 tRFs 的初步研究可能为探索 CD5+R/R DLBCL 的发病机制和进展提供了有价值的方法。

审稿人

叶振清、Raju Nagarajan 和 窦金庄。

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