Evidence map›Paper›PMID 24566139›Full record

ArticleInternational journal of molecular sciences2014

A genotoxic stress-responsive miRNA, miR-574-3p, delays cell growth by suppressing the enhancer of rudimentary homolog gene in vitro.

Ken-ichi Ishikawa, Atsuko Ishikawa, Yoshimi Shoji, Takashi Imai

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. ERH Gene and Its Role in Cancer Cells.Frontiers in oncology · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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  12. Review
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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

4 authors at 1 institution in 1 country.

Ken-ichi IshikawaAdvanced Radiation Biology Research Program, Research Center for Charged Particle Therapy, National Institute for Radiological Sciences, Anagawa 4-9-1, Inage, Chiba 263-8555, Japan. k_ishi@nirs.go.jp.
Atsuko IshikawaAdvanced Radiation Biology Research Program, Research Center for Charged Particle Therapy, National Institute for Radiological Sciences, Anagawa 4-9-1, Inage, Chiba 263-8555, Japan. a_ishi@nirs.go.jp.
Yoshimi ShojiAdvanced Radiation Biology Research Program, Research Center for Charged Particle Therapy, National Institute for Radiological Sciences, Anagawa 4-9-1, Inage, Chiba 263-8555, Japan. y_otsuka@nirs.go.jp.
Takashi ImaiAdvanced Radiation Biology Research Program, Research Center for Charged Particle Therapy, National Institute for Radiological Sciences, Anagawa 4-9-1, Inage, Chiba 263-8555, Japan. imait@nirs.go.jp.
National Institute for Materials Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA (miRNA) is a type of non-coding RNA that regulates the expression of its target genes by interacting with the complementary sequence of the target mRNA molecules. Recent evidence has shown that genotoxic stress induces miRNA expression, but the target genes involved and role in cellular responses remain unclear. We examined the role of miRNA in the cellular response to X-ray irradiation by studying the expression profiles of radio-responsive miRNAs and their target genes in cultured human cell lines. We found that expression of miR-574-3p was induced in the lung cancer cell line A549 by X-ray irradiation. Overexpression of miR-574-3p caused delayed growth in A549 cells. A predicted target site was detected in the 3'-untranslated region of the enhancer of the rudimentary homolog (ERH) gene, and transfected cells showed an interaction between the luciferase reporter containing the target sequences and miR-574-3p. Overexpression of miR-574-3p suppressed ERH protein production and delayed cell growth. This delay was confirmed by knockdown of ERH expression. Our study suggests that miR-574-3p may contribute to the regulation of the cell cycle in response to X-ray irradiation via suppression of ERH protein production.

Indexed as

3' Untranslated RegionsCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCell ProliferationDNA DamageDown-RegulationHumansMicroRNAsRNA InterferenceRNA, Small InterferingTranscription FactorsX-Rays3' Untranslated RegionsCell Cycle ProteinsERH protein, humanMicroRNAsMIRN574 microRNA, humanRNA, Small InterferingTranscription Factors

Identifiers

PMID24566139
PMCPMC3958894
OpenAlexW2006751624

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.