HIV-1 Vpr protein upregulates microRNA-210-5p expression to induce G2 arrest by targeting TGIF2

Zhao, Richard Y. and Qiao, Jialu and Peng, Qian and Qian, Feng and You, Qiang and Feng, Lingyan and Hu, Song and Liu, Wei and Huang, Lixia and Shu, Xiji and Sun, Binlian (2021) HIV-1 Vpr protein upregulates microRNA-210-5p expression to induce G2 arrest by targeting TGIF2. PLOS ONE, 16 (12). e0261971. ISSN 1932-6203

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Abstract

MicroRNAs (miRNAs) are important molecules that mediate virus-host interactions, mainly by regulating gene expression via gene silencing. Here, we demonstrated that HIV-1 infection upregulated miR-210-5p in HIV-1-inoculated cell lines and in the serum of HIV-1-infected individuals. Luciferase reporter assays and western blotting confirmed that a target protein of miR-210-5p, TGIF2, is regulated by HIV-1 infection. Furthermore, HIV-1 Vpr protein induced miR-210-5p expression. The use of a miR-210-5p inhibitor and TGIF2 overexpression showed that Vpr upregulated miR-210-5p and thereby downregulated TGIF2, which might be one of the mechanisms used by Vpr to induce G2 arrest. Moreover, we identified a transcription factor, NF-κB p50, which upregulated miR-210-5p in response to Vpr protein. In conclusion, we identified a mechanism whereby miR-210-5p, which is induced upon HIV-1 infection, targets TGIF2. This pathway was initiated by Vpr protein activating NF-κB p50, which promoted G2 arrest. These alterations orchestrated by miRNA provide new evidence on how HIV-1 interacts with its host during infection and increase our understanding of the mechanism by which Vpr regulates the cell cycle.

Item Type: Article
Subjects: Oalibrary Press > Biological Science
Depositing User: Managing Editor
Date Deposited: 22 Dec 2022 12:46
Last Modified: 10 Nov 2023 05:02
URI: http://asian.go4publish.com/id/eprint/265

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