Evidence map›Paper›PMID 36005825›Full record

ArticleNon-coding RNA2022

SV40 miR-S1 and Cellular miR-1266 Sequester Each Other from Their Targets, Enhancing Telomerase Activity and Viral Replication.

Tetsuyuki Takahashi, Hirona Ichikawa, Yukiko Okayama, Manami Seki, Takao Hijikata

Open access · goldAbstract read
In one paragraph

Article in Non-coding RNA, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 41% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Tetsuyuki TakahashiDepartment of Anatomy and Cell Biology, Research Institute of Pharmaceutical Science, Faculty of Pharmacy, Musashino University, Tokyo 202-8585, Japan.
Hirona IchikawaDepartment of Anatomy and Cell Biology, Research Institute of Pharmaceutical Science, Faculty of Pharmacy, Musashino University, Tokyo 202-8585, Japan.
Yukiko OkayamaDepartment of Anatomy and Cell Biology, Research Institute of Pharmaceutical Science, Faculty of Pharmacy, Musashino University, Tokyo 202-8585, Japan.
Manami SekiDepartment of Anatomy and Cell Biology, Research Institute of Pharmaceutical Science, Faculty of Pharmacy, Musashino University, Tokyo 202-8585, Japan.
Takao HijikataDepartment of Anatomy and Cell Biology, Research Institute of Pharmaceutical Science, Faculty of Pharmacy, Musashino University, Tokyo 202-8585, Japan.
Musashino University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Virus-encoded microRNAs (miRNAs) target viral and host mRNAs to repress protein production from viral and host genes, and regulate viral persistence, cell transformation, and evasion of the immune system. The present study demonstrated that simian virus 40 (SV40)-encoded miRNA miR-S1 targets a cellular miRNA miR-1266 to derepress their respective target proteins, namely, T antigens (Tags) and telomerase reverse transcriptase (TERT). An in silico search for cellular miRNAs to interact with viral miR-S1 yielded nine potential miRNAs, five of which, including miR-1266, were found to interact with miR-S1 in dual-luciferase tests employing reporter plasmids containing the miRNA sequences with miR-S1. Intracellular bindings of miR-1266 to miR-S1 were also verified by the pull-down assay. These miRNAs were recruited into the Ago2-associated RNA-induced silencing complex. Intracellular coexpression of miR-S1 with miR-1266 abrogated the downregulation of TERT and decrease in telomerase activity induced by miR-1266. These effects of miR-S1 were also observed in miR-1266-expressing A549 cells infected with SV40. Moreover, the infected cells contained more Tag, replicated more viral DNA, and released more viral particles than control A549 cells infected with SV40, indicating that miR-S1-induced Tag downregulation was antagonized by miR-1266. Collectively, the present results revealed an interplay of viral and cellular miRNAs to sequester each other from their respective targets. This is a novel mechanism for viruses to manipulate the expression of viral and cellular proteins, contributing to not only viral lytic and latent replication but also cell transformation observed in viral infectious diseases including oncogenesis.

Indexed as

interplaymiR-1266miRNAmiR-S1simian virus 40

Identifiers

PMID36005825
PMCPMC9413689
OpenAlexW4288717978

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.