Differential microRNA Expression in Newcastle Disease Virus-Infected HeLa Cells and Its Role in Regulating Virus Replication.

Differential microRNA Expression in Newcastle Disease Virus-Infected HeLa Cells and Its Role in Regulating Virus Replication.
复制标题

新城疫病毒感染的 HeLa 细胞中差异 microRNA 表达及其在调节病毒复制中的作用

DOI:
10.3389/fonc.2021.616809
复制
发表时间:
2021
影响因子:
4.7
通讯作者:
Liu X
Liu X
中科院分区:
医学3区
文献类型:
--
作者:
Chen Y;Zhu S;Pei Y;Hu J;Hu Z;Liu X;Wang X;Gu M;Hu S;Liu X

文献摘要

参考文献

被引文献

相似文献

新城疫病毒(NDV)是一种溶瘤病毒,能特异性杀伤肿瘤细胞,是一种极具吸引力的肿瘤溶瘤剂。病毒感染可引起细胞内微小RNA(MiRNA)表达谱的改变,从而极大地影响病毒的复制和致病。然而,新城疫病毒复制和肿瘤细胞miRNA表达之间的相互作用在很大程度上仍不清楚。在本研究中,我们通过小RNA深度测序比较了未感染和感染新城疫病毒的HeLa细胞中细胞miRNAs的谱。在此,我们报道了新城疫病毒感染HeLa细胞后,感染后6h的40miRNAs和12hPI的62miRNAs的水平发生了显著的变化。在23个高度差异表达的miRNAs中,NDV感染在两个时间点均显著上调了3个miRNAs的水平,抑制了20个miRNAs的水平。这23个miRNAs被认为是针对与病毒复制和抗病毒免疫有关的各种基因,如ErbB、Jak-STAT、NF-kB和RIG-I样受体。通过定量RT-PCR对深度测序结果进行验证,从该23-miRNA文库中随机选择的10个miRNAs中有9个与深度测序数据一致,其中6个下调,3个上调。进一步的功能研究表明,这个23-miRNA池中的一个成分hsa-miR-4521可以抑制新城疫病毒在HeLa细胞中的复制。此外,双重荧光素酶和基因表达阵列发现,序列相似性129的成员A(FAM129A)直接被hsa-miR-4521靶向并正向调控新城疫病毒在HeLa细胞中的复制,表明hsa-miR-4521可能通过与FAM129A相互作用来调节新城疫病毒的复制。据我们所知,这是首次报道了新城疫病毒感染后肿瘤细胞中miRNA的动态表达谱,为进一步研究miRNAs在新城疫病毒介导的肿瘤分解中的作用提供了有价值的基础。
As an oncolytic virus, Newcastle disease virus (NDV) can specifically kill tumor cells and has been tested as an attractive oncolytic agent for cancer virotherapy. Virus infection can trigger the changes of the cellular microRNA (miRNA) expression profile, which can greatly influence viral replication and pathogenesis. However, the interplay between NDV replication and cellular miRNA expression in tumor cells is still largely unknown. In the present study, we compared the profiles of cellular miRNAs in uninfected and NDV-infected HeLa cells by small RNA deep sequencing. Here we report that NDV infection in HeLa cells significantly changed the levels of 40 miRNAs at 6 h post-infection (hpi) and 62 miRNAs at 12 hpi. Among 23 highly differentially expressed miRNAs, NDV infection greatly promoted the levels of 3 miRNAs and suppressed the levels of 20 miRNAs at both time points. These 23 miRNAs are predicted to target various genes involved in virus replication and antiviral immunity such as ErbB, Jak-STAT, NF-kB and RIG-I-like receptor. Verification of deep sequencing results by quantitative RT-PCR showed that 9 out of 10 randomly selected miRNAs chosen from this 23-miRNA pool were consistent with deep sequencing data, including 6 down-regulated and 3 up-regulated. Further functional research revealed that hsa-miR-4521, a constituent in this 23-miRNA pool, inhibited NDV replication in HeLa cells. Moreover, dual-luciferase and gene expression array uncovered that the member A of family with sequence similarity 129 (FAM129A) was directly targeted by hsa-miR-4521 and positively regulated NDV replication in HeLa cells, indicating that hsa-miR-4521 may regulate NDV replication via interaction with FAM129A. To our knowledge, this is the first report of the dynamic cellular miRNA expression profile in tumor cells after NDV infection and may provide a valuable basis for further investigation on the roles of miRNAs in NDV-mediated oncolysis.
DOI: 10.1186/s40064-015-1601-7
发表时间: 2016
期刊: SpringerPlus
影响因子: --
作者:
Gunzer K;Joly F;Ferrero JM;Gligorov J;de Mont-Serrat H;Uttenreuther-Fischer M;Pelling K;Wind S;Bousquet G;Misset JL
通讯作者: Misset JL
DOI: 10.1097/jto.0b013e3181f77a53
发表时间: 2010-12
期刊: Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
影响因子: --
作者:
Hoque MO;Brait M;Rosenbaum E;Poeta ML;Pal P;Begum S;Dasgupta S;Carvalho AL;Ahrendt SA;Westra WH;Sidransky D
通讯作者: Sidransky D
DOI: 10.18632/genesandcancer.162
发表时间: 2017-11
期刊: Genes & cancer
影响因子: --
作者:
Geethadevi A;Parashar D;Bishop E;Pradeep S;Chaluvally-Raghavan P
通讯作者: Chaluvally-Raghavan P
DOI: 10.3390/cancers12061450
发表时间: 2020-06-01
期刊: CANCERS
影响因子: 5.2
作者:
Dias, Francisca;Teixeira, Ana Luisa;Medeiros, Rui
通讯作者: Medeiros, Rui
DOI: 10.1245/s10434-018-6626-z
发表时间: 2018-09-01
影响因子: 3.7
作者:
Chiam, Karen;Mayne, George C.;Hussey, Damian J.
通讯作者: Hussey, Damian J.