Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation

Non-coding RNAs represent a class of important regulators in immune response. Previously, LINC02605 was identified as a candidate regulator in innate immune response by lncRNA microarray assays. In this study, we systematically analyzed the functions and the acting mechanisms of LINC02605 in antivir...

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Autores principales:	Rui Xu, Shuang-Shuang Yu, Ran-Ran Yao, Rong-Chun Tang, Jia-Wei Liang, Xuewen Pang, Jun Zhang
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	LINC02605 type I IFNs hsa-miR-107 PTEN IRF3 nuclear translocation Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/7a62eee2442549e2b945cc547e14b534
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spelling	oai:doaj.org-article:7a62eee2442549e2b945cc547e14b5342021-11-05T10:51:01ZInterferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation1664-322410.3389/fimmu.2021.755512https://doaj.org/article/7a62eee2442549e2b945cc547e14b5342021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.755512/fullhttps://doaj.org/toc/1664-3224Non-coding RNAs represent a class of important regulators in immune response. Previously, LINC02605 was identified as a candidate regulator in innate immune response by lncRNA microarray assays. In this study, we systematically analyzed the functions and the acting mechanisms of LINC02605 in antiviral innate immune response. LINC02605 was up-regulated by RNA virus, DNA virus, and type I IFNs in NF-κB and Jak-stat dependent manner. Overexpression of LINC02605 promotes RNA virus-induced type I interferon production and inhibited viral replication. Consistently, knockdown of LINC02605 resulted in reduced antiviral immune response and increased viral replication. Mechanistically, LINC02605 released the inhibition of hsa-miR-107 on the expression of phosphatase and tensin homolog (PTEN). By microRNA mimics and inhibitors, hsa-miR-107 was demonstrated to not only inhibit PTEN’s expression but also negatively regulate the antiviral immune response. Knockdown of LINC02605 led to the reduction of PTEN expression both in mRNA and protein levels. Overexpression of LINC02605 had an opposite impact. Moreover, LINC02605 attenuated the serine 97 phosphorylation level of interferon regulatory factor 3 (IRF3) by promoting PTEN expression. Nucleoplasmic fragmentation assay showed that knocking down LINC02605 inhibited the nuclear translocation of IRF3, rendering the host cells more susceptible to viral invasion, while overexpression showed opposite effects. Therefore, LINC02605 is an induced lncRNA by viral infection and plays a positive feedback in antiviral immune response through modulating the nuclear translocation of IRF3.Rui XuShuang-Shuang YuRan-Ran YaoRong-Chun TangJia-Wei LiangXuewen PangJun ZhangFrontiers Media S.A.articleLINC02605type I IFNshsa-miR-107PTENIRF3nuclear translocationImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	LINC02605 type I IFNs hsa-miR-107 PTEN IRF3 nuclear translocation Immunologic diseases. Allergy RC581-607
spellingShingle	LINC02605 type I IFNs hsa-miR-107 PTEN IRF3 nuclear translocation Immunologic diseases. Allergy RC581-607 Rui Xu Shuang-Shuang Yu Ran-Ran Yao Rong-Chun Tang Jia-Wei Liang Xuewen Pang Jun Zhang Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation
description	Non-coding RNAs represent a class of important regulators in immune response. Previously, LINC02605 was identified as a candidate regulator in innate immune response by lncRNA microarray assays. In this study, we systematically analyzed the functions and the acting mechanisms of LINC02605 in antiviral innate immune response. LINC02605 was up-regulated by RNA virus, DNA virus, and type I IFNs in NF-κB and Jak-stat dependent manner. Overexpression of LINC02605 promotes RNA virus-induced type I interferon production and inhibited viral replication. Consistently, knockdown of LINC02605 resulted in reduced antiviral immune response and increased viral replication. Mechanistically, LINC02605 released the inhibition of hsa-miR-107 on the expression of phosphatase and tensin homolog (PTEN). By microRNA mimics and inhibitors, hsa-miR-107 was demonstrated to not only inhibit PTEN’s expression but also negatively regulate the antiviral immune response. Knockdown of LINC02605 led to the reduction of PTEN expression both in mRNA and protein levels. Overexpression of LINC02605 had an opposite impact. Moreover, LINC02605 attenuated the serine 97 phosphorylation level of interferon regulatory factor 3 (IRF3) by promoting PTEN expression. Nucleoplasmic fragmentation assay showed that knocking down LINC02605 inhibited the nuclear translocation of IRF3, rendering the host cells more susceptible to viral invasion, while overexpression showed opposite effects. Therefore, LINC02605 is an induced lncRNA by viral infection and plays a positive feedback in antiviral immune response through modulating the nuclear translocation of IRF3.
format	article
author	Rui Xu Shuang-Shuang Yu Ran-Ran Yao Rong-Chun Tang Jia-Wei Liang Xuewen Pang Jun Zhang
author_facet	Rui Xu Shuang-Shuang Yu Ran-Ran Yao Rong-Chun Tang Jia-Wei Liang Xuewen Pang Jun Zhang
author_sort	Rui Xu
title	Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation
title_short	Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation
title_full	Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation
title_fullStr	Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation
title_full_unstemmed	Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation
title_sort	interferon-inducible linc02605 promotes antiviral innate responses by strengthening irf3 nuclear translocation
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/7a62eee2442549e2b945cc547e14b534
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Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation

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