Evidence map›Paper›PMID 23437304›Full record

ArticlePloS one2013

MicroRNA-18a attenuates DNA damage repair through suppressing the expression of ataxia telangiectasia mutated in colorectal cancer.

Chung-Wah Wu, Yu-Juan Dong, Qiao-Yi Liang, Xin-Qi He, Simon S M Ng, Francis K L Chan, Joseph J Y Sung, Jun Yu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Review
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  6. Review
  7. Article
  8. Review
  9. MicroRNAs and Apoptosis in Colorectal Cancer.International journal of molecular sciences · 2020
    Review
  10. Function and mechanisms of microRNA-20a in colorectal cancer.Experimental and therapeutic medicine · 2020
    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

8 authors at 2 institutions in 1 country.

Chung-Wah WuInstitute of Digestive Disease and Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, Special Administrative Region, People's Republic of China.
Yu-Juan Dong
Qiao-Yi Liang
Xin-Qi He
Simon S M Ng
Francis K L Chan
Joseph J Y Sung
Jun Yu
Chinese University of Hong Kong · CNChinese University of Hong Kong, Shenzhen · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundmiR-18a is one of the most up-regulated miRNAs in colorectal cancers (CRC) based on miRNA profiling. In this study, we examined the functional significance of miR-18a in CRC.

methodsExpression of miR-18a was investigated in 45 CRC patients. Potential target genes of miR-18a were predicted by in silico search and confirmed by luciferase activity assay and Western blot. DNA damage was measured by comet assay. Gene function was measured by cell viability, colony formation and apoptosis assays.

resultsThe up-regulation of miR-18a was validated and confirmed in 45 primary CRC tumors compared with adjacent normal tissues (p<0.0001). Through in silico search, the 3'UTR of Ataxia telangiectasia mutated (ATM) contains a conserved miR-18a binding site. Expression of ATM was down-regulated in CRC tumors (p<0.0001) and inversely correlated with miR-18a expression (r = -0.4562, p<0.01). Over-expression of miR-18a in colon cancer cells significantly reduced the luciferase activity of the construct with wild-type ATM 3'UTR but not that with mutant ATM 3'UTR, inferring a direct interaction of miR-18a with ATM 3'UTR. This was further confirmed by the down-regulation of ATM protein by miR-18a. As ATM is a key enzyme in DNA damage repair, we evaluated the effect of miR-18a on DNA double-strand breaks. Ectopic expression of miR-18a significantly inhibited the repair of DNA damage induced by etoposide (p<0.001), leading to accumulation of DNA damage, increase in cell apoptosis and poor clonogenic survival.

conclusionmiR-18a attenuates cellular repair of DNA double-strand breaks by directly suppressing ATM, a key enzyme in DNA damage repair.

Indexed as

DNA DamageGene Expression Regulation, Neoplastic3' Untranslated RegionsAgedAged, 80 and overApoptosisAtaxia Telangiectasia Mutated ProteinsBase PairingBase SequenceCell Cycle ProteinsCell Line, TumorColorectal NeoplasmsDNA-Binding ProteinsDNA Breaks, Double-StrandedEtoposideFemale3' Untranslated RegionsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA-Binding ProteinsEtoposideMicroRNAsMIRN18 microRNA, humanProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID23437304
PMCPMC3578802
OpenAlexW1978162793

What OpenQuestion holds

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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.