Mir-302c mediates influenza A virus-induced IFNβ expression by targeting NF-κB inducing kinase

Shulin Gui; Xueyuan Chen; Mo Zhang; Fanpeng Zhao; Yushun Wan; Li Wang; Gang Xu; Li Zhou; Xin Yue; Ying Zhu; Shi Liu

doi:10.1016/j.febslet.2015.11.011

Mir-302c mediates influenza A virus-induced IFNβ expression by targeting NF-κB inducing kinase

Shulin Gui, Xueyuan Chen, Mo Zhang, Fanpeng Zhao, Yushun Wan, Li Wang, Gang Xu, Li Zhou, Xin Yue, Ying Zhu, Shi Liu

Research output: Contribution to journal › Article › peer-review

43 Scopus citations

Abstract

Little is known about the role of microRNA during influenza A virus (IAV) infection. We observed that NIK 3′UTR luciferase activity was elevated during IAV infection. Further studies demonstrated that miR-302c reduced NIK expression, resulting in the reduction of IFNβ mRNA expression. We found that miR-302c prevented the translocation of NF-κB from the cytosol to the nucleus. Furthermore, IAV infection downregulated miR-302c expression, leading to the activation of IFNβ expression and the inhibition of viral replication. Compared to miR-302c, miR-520e cannot promote viral replication and production, although the two microRNAs target the same site of the NIK 3′UTR. Collectively, our work defines a novel signaling pathway implicated in the control of IFNβ mRNA expression during IAV infection.

Original language	English (US)
Pages (from-to)	4112-4118
Number of pages	7
Journal	FEBS Letters
Volume	589
Issue number	24
DOIs	https://doi.org/10.1016/j.febslet.2015.11.011
State	Published - Dec 21 2015
Externally published	Yes

Bibliographical note

Publisher Copyright:
© 2015 Federation of European Biochemical Societies.

Keywords

Influenza A virus
Innate immune
MiR-302c
NF-κB-inducing kinase
Type I IFN

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.febslet.2015.11.011

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title = "Mir-302c mediates influenza A virus-induced IFNβ expression by targeting NF-κB inducing kinase",

abstract = "Little is known about the role of microRNA during influenza A virus (IAV) infection. We observed that NIK 3′UTR luciferase activity was elevated during IAV infection. Further studies demonstrated that miR-302c reduced NIK expression, resulting in the reduction of IFNβ mRNA expression. We found that miR-302c prevented the translocation of NF-κB from the cytosol to the nucleus. Furthermore, IAV infection downregulated miR-302c expression, leading to the activation of IFNβ expression and the inhibition of viral replication. Compared to miR-302c, miR-520e cannot promote viral replication and production, although the two microRNAs target the same site of the NIK 3′UTR. Collectively, our work defines a novel signaling pathway implicated in the control of IFNβ mRNA expression during IAV infection.",

keywords = "Influenza A virus, Innate immune, MiR-302c, NF-κB-inducing kinase, Type I IFN",

author = "Shulin Gui and Xueyuan Chen and Mo Zhang and Fanpeng Zhao and Yushun Wan and Li Wang and Gang Xu and Li Zhou and Xin Yue and Ying Zhu and Shi Liu",

note = "Publisher Copyright: {\textcopyright} 2015 Federation of European Biochemical Societies.",

year = "2015",

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day = "21",

doi = "10.1016/j.febslet.2015.11.011",

language = "English (US)",

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T1 - Mir-302c mediates influenza A virus-induced IFNβ expression by targeting NF-κB inducing kinase

AU - Gui, Shulin

AU - Chen, Xueyuan

AU - Zhang, Mo

AU - Zhao, Fanpeng

AU - Wan, Yushun

AU - Wang, Li

AU - Xu, Gang

AU - Zhou, Li

AU - Yue, Xin

AU - Zhu, Ying

AU - Liu, Shi

PY - 2015/12/21

Y1 - 2015/12/21

N2 - Little is known about the role of microRNA during influenza A virus (IAV) infection. We observed that NIK 3′UTR luciferase activity was elevated during IAV infection. Further studies demonstrated that miR-302c reduced NIK expression, resulting in the reduction of IFNβ mRNA expression. We found that miR-302c prevented the translocation of NF-κB from the cytosol to the nucleus. Furthermore, IAV infection downregulated miR-302c expression, leading to the activation of IFNβ expression and the inhibition of viral replication. Compared to miR-302c, miR-520e cannot promote viral replication and production, although the two microRNAs target the same site of the NIK 3′UTR. Collectively, our work defines a novel signaling pathway implicated in the control of IFNβ mRNA expression during IAV infection.

AB - Little is known about the role of microRNA during influenza A virus (IAV) infection. We observed that NIK 3′UTR luciferase activity was elevated during IAV infection. Further studies demonstrated that miR-302c reduced NIK expression, resulting in the reduction of IFNβ mRNA expression. We found that miR-302c prevented the translocation of NF-κB from the cytosol to the nucleus. Furthermore, IAV infection downregulated miR-302c expression, leading to the activation of IFNβ expression and the inhibition of viral replication. Compared to miR-302c, miR-520e cannot promote viral replication and production, although the two microRNAs target the same site of the NIK 3′UTR. Collectively, our work defines a novel signaling pathway implicated in the control of IFNβ mRNA expression during IAV infection.

KW - Influenza A virus

KW - Innate immune

KW - MiR-302c

KW - NF-κB-inducing kinase

KW - Type I IFN

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DO - 10.1016/j.febslet.2015.11.011

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SN - 0014-5793

VL - 589

SP - 4112

EP - 4118

JO - FEBS Letters

JF - FEBS Letters

IS - 24

ER -

Mir-302c mediates influenza A virus-induced IFNβ expression by targeting NF-κB inducing kinase

Abstract

Bibliographical note

Keywords

UN SDGs

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