Evidence map›Paper›PMID 26744345›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2016

MiR-613 induces cell cycle arrest by targeting CDK4 in non-small cell lung cancer.

Duo Li, Dong-Qiong Li, Dan Liu, Xiao-Jun Tang

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2016. 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
2.9field-weighted citation impact, top 10% 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, 44 citations in OpenAlex.

  1. [Research Progress of Engineered Exosomes in the Treatment of Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024
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  12. Non-Coding RNAs in Lung Tumor Initiation and Progression.International journal of molecular sciences · 2020
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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 2 institutions in 1 country.

Duo LiThe 2nd Department of Respiratory Disease, The Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan, 646000, China.
Dong-Qiong LiThe 2nd Department of Respiratory Disease, The Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan, 646000, China.
Dan LiuIntensive Care Unit, The Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan, 646000, China.
Xiao-Jun TangThoracic Surgery Department, The Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan, 646000, China. tangxj2014@126.com.
Southwest Medical University · CNFirst Affiliated Hospital of Sichuan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDeregulation of microRNAs (miRNAs) has been associated with a variety of cancers, including non-small cell lung cancer (NSCLC). Here, we investigated anomalous miR-613 expression and its possible functional consequences in primary NSCLC samples and NSCLC-derived cell lines.

methodsThe expression of miR-613 was measured by quantitative RT-PCR in 56 primary NSCLC tissues and adjacent non-tumor tissues. The effect of miR-613 up- or down-regulation in NSCLC-derived cells was evaluated in vitro by cell viability and colony formation assays and in vivo by growth assays in xenografted nude mice.

resultsUsing quantitative RT-PCR, we found that miR-613 was down-regulated in 76.8 % (43/56) of the primary NSCLC tissues tested when compared to the adjacent non-tumor tissues. We also found that the miR-613 mimic used reduced in vitro cell viability and colony formation by inducing cell cycle arrest in NSCLC-derived cells, and inhibited in vivo tumor cell growth in xenografted nude mice. Inversely, we found that the miR-613 inhibitor used increased the viability and colony forming capacity of NSCLC-derived cells and tumor cell growth in xenografted nude mice. In addition, we identified CDK4 as a potential target of miR-613 using in silico Miranda predictions. Subsequent dual-luciferase reporter assays revealed that CDK4 acts as a direct target of miR-613. Concordantly, we found that both miR-613 mimics and inhibitors could decrease and increase CDK4 protein levels in NSCLC-derived cells, respectively.

conclusionsFrom our results we conclude that miR-613 may act as a tumor suppressor in NSCLC and may serve as a tool for miRNA-based NSCLC therapy.

Indexed as

Cell Cycle CheckpointsAdultAgedAnimalsBase SequenceCarcinoma, Non-Small-Cell LungCell ProliferationCyclin-Dependent Kinase 4Down-RegulationFemaleGene Knockdown TechniquesHumansLung NeoplasmsMaleMice, NudeMicroRNAsCDK4 protein, humanCyclin-Dependent Kinase 4MicroRNAsMIRN613 microRNA, humanCDK4Cell cycleLung cancermiR-613

Identifiers

PMID26744345
PMCPMC13001875
OpenAlexW2228454978

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.