Evidence map›Paper›PMID 26115122›Full record

ArticlePloS one2015

The Effect of MicroRNA-124 Overexpression on Anti-Tumor Drug Sensitivity.

Shiau-Mei Chen, Wen-Cheng Chou, Ling-Yueh Hu, Chia-Ni Hsiung, Hou-Wei Chu, Yuan-Ling Huang, Huan-Ming Hsu, Jyh-Cherng Yu, Chen-Yang Shen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

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  14. miRNA signatures in childhood sarcomas and their clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
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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

9 authors at 3 institutions in 1 country.

Shiau-Mei ChenGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Wen-Cheng ChouInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Ling-Yueh HuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Chia-Ni HsiungInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Hou-Wei ChuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Yuan-Ling HuangGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Huan-Ming HsuDepartment of Surgery, Tri-Service General Hospital, Taipei, Taiwan.
Jyh-Cherng YuDepartment of Surgery, Tri-Service General Hospital, Taipei, Taiwan.
Chen-Yang ShenGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; College of Public Health, China Medical University, Taichong, Taiwan.
Institute of Biomedical Sciences, Academia Sinica · TWTri-Service General Hospital · TWChina Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs play critical roles in regulating various physiological processes, including growth and development. Previous studies have shown that microRNA-124 (miR-124) participates not only in regulation of early neurogenesis but also in suppression of tumorigenesis. In the present study, we found that overexpression of miR-124 was associated with reduced DNA repair capacity in cultured cancer cells and increased sensitivity of cells to DNA-damaging anti-tumor drugs, specifically those that cause the formation of DNA strand-breaks (SBs). We then examined which DNA repair-related genes, particularly the genes of SB repair, were regulated by miR-124. Two SB repair-related genes, encoding ATM interactor (ATMIN) and poly (ADP-ribose) polymerase 1 (PARP1), were strongly affected by miR-124 overexpression, by binding of miR-124 to the 3¢-untranslated region of their mRNAs. As a result, the capacity of cells to repair DNA SBs, such as those resulting from homologous recombination, was significantly reduced upon miR-124 overexpression. A particularly important therapeutic implication of this finding is that overexpression of miR-124 enhanced cell sensitivity to multiple DNA-damaging agents via ATMIN- and PARP1-mediated mechanisms. The translational relevance of this role of miR-124 in anti-tumor drug sensitivity is suggested by the finding that increased miR-124 expression correlates with better breast cancer prognosis, specifically in patients receiving chemotherapy. These findings suggest that miR-124 could potentially be used as a therapeutic agent to improve the efficacy of chemotherapy with DNA-damaging agents.

Indexed as

Gene ExpressionAntineoplastic AgentsBreast NeoplasmsCell Line, TumorDNA RepairDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsNeoplasmsOsteosarcomaPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesPrognosisRNA InterferenceAntineoplastic AgentsATMIN protein, humanMicroRNAsMIRN124 microRNA, humanPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesRNA, MessengerTranscription Factors

Identifiers

PMID26115122
PMCPMC4482746
OpenAlexW2147372837

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.