Evidence map›Paper›PMID 28537886›Full record

ArticleOncotarget2017

ADAM9 enhances CDCP1 by inhibiting miR-1 through EGFR signaling activation in lung cancer metastasis.

Kuo-Liang Chiu, Yu-Sen Lin, Ting-Ting Kuo, Chia-Chien Lo, Yu-Kai Huang, Hsien-Fang Chang, Eric Y Chuang, Ching-Chan Lin, Wei-Chung Cheng, Yen-Nien Liu and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

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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

12 authors at 4 institutions in 1 country.

Kuo-Liang ChiuGraduate Institute of Clinical Medical Science, China Medical University, Taichung 404, Taiwan.
Yu-Sen LinGraduate Institute of Clinical Medical Science, China Medical University, Taichung 404, Taiwan.
Ting-Ting KuoCenter for Molecular Medicine, China Medical University Hospital, Taichung 404, Taiwan.
Chia-Chien LoCenter for Molecular Medicine, China Medical University Hospital, Taichung 404, Taiwan.
Yu-Kai HuangCenter for Molecular Medicine, China Medical University Hospital, Taichung 404, Taiwan.
Hsien-Fang ChangBioinformatics and Biostatistics Core, Center of Genomic Medicine, National Taiwan University, Taipei 100, Taiwan.
Eric Y ChuangBioinformatics and Biostatistics Core, Center of Genomic Medicine, National Taiwan University, Taipei 100, Taiwan.
Ching-Chan LinGraduate Institute of Clinical Medical Science, China Medical University, Taichung 404, Taiwan.
Wei-Chung ChengGraduate Institute of BioMedical Sciences, China Medical University, Taichung 404, Taiwan.
Yen-Nien LiuGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan.
Liang-Chuan LaiBioinformatics and Biostatistics Core, Center of Genomic Medicine, National Taiwan University, Taipei 100, Taiwan.
Yuh-Pyng SherGraduate Institute of Clinical Medical Science, China Medical University, Taichung 404, Taiwan.
China Medical University · TWNational Taiwan University · TWChina Medical University Hospital · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs), which are endogenous short noncoding RNAs, can regulate genes involved in important biological and pathological functions. Therefore, dysregulation of miRNAs plays a critical role in cancer progression. However, whether the aberrant expression of miRNAs is regulated by oncogenes remains unclear. We previously demonstrated that a disintegrin and metalloprotease domain 9 (ADAM9) promotes lung metastasis by enhancing the expression of a pro-migratory protein, CUB domain containing protein 1 (CDCP1). In this study, we found that this process occurred via miR-1 down-regulation. miR-1 expression was down-regulated in lung tumors, but increased in ADAM9-knockdown lung cancer cells, and was negatively correlated with CDCP1 expression as well as the migration ability of lung cancer cells. Luciferase-based reporter assays showed that miR-1 directly bound to the 3'-untranslated region of CDCP1 and inhibited its translation. Treatment with a miR-1 inhibitor restored CDCP1 protein levels and enhanced tumor cell mobility. Overexpression of miR-1 decreased tumor metastases and increased the survival rate in mice. ADAM9 knockdown reduced EGFR signaling and increased miR-1 expression. These results revealed that ADAM9 down-regulates miR-1 via activating EGFR signaling pathways, which in turn enhances CDCP1 expression to promote lung cancer progression.

Indexed as

Signal Transduction3' Untranslated RegionsADAM ProteinsAnimalsAntigens, CDAntigens, NeoplasmCell Adhesion MoleculesCell Line, TumorCell MovementDisease Models, AnimalDisease ProgressionErbB ReceptorsGene Expression Regulation, NeoplasticHeterograftsHumansLung Neoplasms3' Untranslated RegionsADAM9 protein, humanADAM ProteinsAntigens, CDAntigens, NeoplasmCDCP1 protein, humanCell Adhesion MoleculesErbB ReceptorsMembrane ProteinsMicroRNAsMIRN1 microRNA, humanNeoplasm ProteinsADAM9CDCP1EGFRlung cancermiR-1

Identifiers

PMID28537886
PMCPMC5564571
OpenAlexW2614078866

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.