TP73-AS1 promotes malignant progression of NK/T cell lymphoma by regulating DKK1 methylation.

Q2 Medicine Journal of Buon Pub Date : 2021-07-01

Hui Zhang, Qianqian Huang

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引用次数: 0

Abstract

Purpose: Long non-coding RNA (lncRNA) TP73-AS1 is abnormally expressed in multiple types of tumors, which is able to mediate tumor cell signals. This study aims to explore the role of TP73-AS1 in affecting biological functions of NK/T-cell lymphoma (NKTCL) and DKK1 methylation.

Methods: TP73-AS1 levels in peripheral blood of NKTCL patients and healthy volunteers was detected by quantitative real-time polymerase chain reaction (qRT-PCR). After knockdown of TP73-AS1, proliferative and migratory abilities in SNK-6 and HANK-1 cells were assessed by cell counting kit-8 (CCK-8) and Transwell assay, respectively. Regulatory effect of TP73-AS1 on DKK1 methylation in NKTCL cells was evaluated through methylation-specific PCR (MSP), dual-luciferase reporter assay and RNA Binding Protein Immunoprecipitation (RIP). Rescue experiments were conducted to further validate the interaction between TP73-AS1 and DKK1.

Results: TP73-AS1 level was higher in peripheral blood of NKTCL patients than that of healthy volunteers. Knockdown of TP73-AS1 in vitro weakened proliferative and migratory functions of NKTCL cells. TP73-AS1 induced methylation of DKK1 promoter through DNMT1/DNMT3, thus regulating NKTCL cell functions.

Conclusions: TP73-AS1 level was higher in peripheral blood of NKTCL patients. Through inducing methylation of DKK1 promoter, TP73-AS1 aggravates the malignant progression of NKTCL.

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TP73-AS1通过调节DKK1甲基化促进NK/T细胞淋巴瘤的恶性进展。

目的:长链非编码RNA (Long non-coding RNA, lncRNA) TP73-AS1在多种肿瘤中异常表达，能够介导肿瘤细胞信号。本研究旨在探讨TP73-AS1在影响NK/ t细胞淋巴瘤(NKTCL)生物学功能和DKK1甲基化中的作用。方法:采用实时荧光定量聚合酶链反应(qRT-PCR)检测NKTCL患者和健康志愿者外周血TP73-AS1水平。敲除TP73-AS1后，分别用细胞计数试剂盒-8 (CCK-8)和Transwell法检测SNK-6和HANK-1细胞的增殖能力和迁移能力。通过甲基化特异性PCR (MSP)、双荧光素酶报告基因检测和RNA结合蛋白免疫沉淀(RIP)检测TP73-AS1对NKTCL细胞DKK1甲基化的调控作用。为了进一步验证TP73-AS1与DKK1之间的相互作用，我们进行了救援实验。结果:NKTCL患者外周血TP73-AS1水平明显高于健康志愿者。体外敲低TP73-AS1可减弱NKTCL细胞的增殖和迁移功能。TP73-AS1通过DNMT1/DNMT3诱导DKK1启动子甲基化，从而调控NKTCL细胞功能。结论:NKTCL患者外周血TP73-AS1水平较高。TP73-AS1通过诱导DKK1启动子甲基化，加重NKTCL的恶性进展。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Buon 医学-肿瘤学

自引率

0.00%

发文量

审稿时长

4-8 weeks

期刊介绍： JBUON aims at the rapid diffusion of scientific knowledge in Oncology. Its character is multidisciplinary, therefore all aspects of oncologic activities are welcome including clinical research (medical oncology, radiation oncology, surgical oncology, nursing oncology, psycho-oncology, supportive care), as well as clinically-oriented basic and laboratory research, cancer epidemiology and social and ethical aspects of cancer. Experts of all these disciplines are included in the Editorial Board. With a rapidly increasing body of new discoveries in clinical therapeutics, the molecular mechanisms that contribute to carcinogenesis, advancements in accurate and early diagnosis etc, JBUON offers a free forum for clinicians and basic researchers to make known promptly their achievements around the world. With this aim JBUON accepts a broad spectrum of articles such as editorials, original articles, reviews, special articles, short communications, commentaries, letters to the editor and correspondence among authors and readers. JBUON keeps the characteristics of its former paper print edition and appears as a bimonthly e-published journal with continuous volume, issue and page numbers.