Evidence map›Paper›PMID 27129166›Full record

ArticleOncotarget2016

Extracellular miR-1246 promotes lung cancer cell proliferation and enhances radioresistance by directly targeting DR5.

Dexiao Yuan, Jinping Xu, Juan Wang, Yan Pan, Jiamei Fu, Yang Bai, Jianghong Zhang, Chunlin Shao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Review
  7. Resistance to Radiotherapy in Cancer.Diseases (Basel, Switzerland) · 2025
    Review
  8. Review
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  10. Article
  11. Relationship between exosomes and cancer: formation, diagnosis, and treatment.International journal of biological sciences · 2025
    Review
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  18. Article
  19. APE1 controls DICER1 expression in NSCLC through miR-33a and miR-130b.Cellular and molecular life sciences : CMLS · 2022
    Article
  20. Review

2 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Dexiao YuanInstitute of Radiation Medicine, Fudan University, Shanghai 200032, China.
Jinping XuInstitute of Radiation Medicine, Fudan University, Shanghai 200032, China.
Juan WangInstitute of Radiation Medicine, Fudan University, Shanghai 200032, China.
Yan PanInstitute of Radiation Medicine, Fudan University, Shanghai 200032, China.
Jiamei FuInstitute of Radiation Medicine, Fudan University, Shanghai 200032, China.
Yang BaiInstitute of Radiation Medicine, Fudan University, Shanghai 200032, China.
Jianghong ZhangInstitute of Radiation Medicine, Fudan University, Shanghai 200032, China.
Chunlin ShaoInstitute of Radiation Medicine, Fudan University, Shanghai 200032, China.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MiRNAs in the circulation have been demonstrated to be a type of signaling molecule involved in intercellular communication but little is known about their role in regulating radiosensitivity. This study aims to investigate the effects of extracellular miRNAs induced by ionizing radiation (IR) on cell proliferation and radiosensitivity. The miRNAs in the conditioned medium (CM) from irradiated and non-irradiated A549 lung cancer cells were compared using a microarray assay and the profiles of 21 miRNAs up and down-regulated by radiation were confirmed by qRT-PCR. One of these miRNAs, miR-1246, was especially abundant outside the cells and had a much higher level compared with that inside of cells. The expressions of miR-1246 in both A549 and H446 cells increased along with irradiation dose and the time post-irradiation. By labeling exosomes and miR-1246 with different fluorescence dyes, it was found that the extracellular miR-1246 could shuttle from its donor cells to other recipient cells by a non-exosome associated pathway. Moreover, the treatments of cells with miR-1246 mimic or its antisense inhibitor showed that the extracellular miR-1246 could enhance the proliferation and radioresistance of lung cancer cells. A luciferase reporter-gene transfer experiment demonstrated that the death receptor 5 (DR5) was the direct target of miR-1246, and the kinetics of DR5 expression was opposite to that of miR-1246 in the irradiated cells. Our results show that the oncogene-like extracellular miR-1246 could act as a signaling messenger between irradiated and non-irradiated cells, more importantly, it contributes to cell radioresistance by directly suppressing the DR5 gene.

Indexed as

Radiation ToleranceA549 CellsBystander EffectCell ProliferationCulture Media, ConditionedDose-Response Relationship, RadiationExosomesGene Expression Regulation, NeoplasticHumansKineticsLung NeoplasmsMicroRNAsReceptors, TNF-Related Apoptosis-Inducing LigandRNA InterferenceSignal TransductionTransfectionCulture Media, ConditionedMicroRNAsMIRN1246 microRNA, humanReceptors, TNF-Related Apoptosis-Inducing LigandTNFRSF10B protein, humanbystander effectDR5 geneexosomesextracellular mR-1246radioresistance

Identifiers

PMID27129166
PMCPMC5078045
OpenAlexW2342420211

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.