Evidence map›Paper›PMID 28978708›Full record

ArticleJournal of virology2017

Suppression of MicroRNA 424 Levels by Human Papillomaviruses Is Necessary for Differentiation-Dependent Genome Amplification.

Shiyuan Hong, Shouqiang Cheng, William Songock, Jason Bodily, Laimonis A Laimins

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Role of miRNA-424 in Cancers.OncoTargets and therapy · 2020
    Review
  8. Review
  9. Review
  10. Review
  11. 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 2 institutions in 1 country.

Shiyuan HongDepartment of Microbiology-Immunology, Northwestern University, Feinberg, School of Medicine, Chicago, Illinois, USA.
Shouqiang ChengDepartment of Microbiology-Immunology, Northwestern University, Feinberg, School of Medicine, Chicago, Illinois, USA.
William SongockDepartment of Microbiology and Immunology, LSU Health Sciences Center, Shreveport, Louisiana, USA.
Jason BodilyDepartment of Microbiology and Immunology, LSU Health Sciences Center, Shreveport, Louisiana, USA.
Laimonis A LaiminsDepartment of Microbiology-Immunology, Northwestern University, Feinberg, School of Medicine, Chicago, Illinois, USA l-laimins@northwestern.edu.
Northwestern University · USLouisiana State University Health Sciences Center Shreveport · US

Funding

REGULATION OF HUMAN PAPILLOMAVIRUS GENE EXPRESSIONR01CA059655 · NCI · UNIVERSITY OF CHICAGO · PI LAIMINS, LAIMONIS A. · 1993 to 2023
$7.4M
Renewal: HPV and the DNA Damage ResponseR01CA142861 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Laimonis A. LAIMINS · 2010 to 2026
$5.2M
ThThe Role of Epithelial-Stromal Communication in the Human Papillomavirus Type 16 Life CycleR01AI118904 · NIAID · LOUISIANA STATE UNIV HSC SHREVEPORT · PI BODILY, JASON M · 2015 to 2019
$1.6M
NCI NIH HHS R01 CA059655NCI NIH HHS R01 CA142861NIAID NIH HHS R01 AI118904
6 · The paper itself

Abstract

High-risk human papillomaviruses (HPVs) link their life cycle to epithelial differentiation and require activation of DNA damage pathways for efficient replication. HPVs modulate the expression of cellular transcription factors, as well as cellular microRNAs (miRNAs) to control these activities. One miRNA that has been reported to be repressed in HPV-positive cancers of the cervix and oropharynx is miR-424. Our studies show that miR-424 levels are suppressed in cell lines that stably maintain HPV 31 or 16 episomes, as well as cervical cancer lines that contain integrated genomes such as SiHa. Introduction of expression vectors for miR-424 reduced both the levels of HPV genomes in undifferentiated cells and amplification upon differentiation. Our studies show that the levels of two putative targets of miR-424 that function in DNA damage repair, CHK1 and Wee1, are suppressed in HPV-positive cells, providing an explanation for why this microRNA is targeted in HPV-positive cells.

Indexed as

Genome, ViralVirus ReplicationAlphapapillomavirusCell Cycle ProteinsCell DifferentiationCells, CulturedCheckpoint Kinase 1FemaleHost-Pathogen InteractionsHumansMicroRNAsNuclear ProteinsOncogene Proteins, ViralPapillomavirus E7 ProteinsProtein-Tyrosine KinasesRepressor ProteinsCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanE6 protein, Human papillomavirus type 16MicroRNAsMIRN424 microrna, humanNuclear ProteinsOncogene Proteins, ViralPapillomavirus E7 ProteinsProtein-Tyrosine KinasesRepressor ProteinsWEE1 protein, humanamplificationcheck pointCHK1DNA damage repairHPVmicroRNA

Identifiers

PMID28978708
PMCPMC5709607
OpenAlexW2761676162

What OpenQuestion holds

Textmetadata
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.