Evidence map›Paper›PMID 24997798›Full record

ArticleMolecular cancer2014

miRNA-200c inhibits invasion and metastasis of human non-small cell lung cancer by directly targeting ubiquitin specific peptidase 25.

Jing Li, Qiang Tan, Mingxia Yan, Lei Liu, Hechun Lin, Fangyu Zhao, Guoliang Bao, Hanwei Kong, Chao Ge, Fanglin Zhang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

75 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Review
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  7. The SUMOylation and ubiquitination crosstalk in cancer.Journal of cancer research and clinical oncology · 2023
    Review
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  16. Role of microRNAs in COVID-19 with implications for therapeutics.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  17. Review
  18. Article
  19. Article
  20. Article

15 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

14 authors at 5 institutions in 1 country.

Jing Li
Qiang Tan
Mingxia Yan
Lei Liu
Hechun Lin
Fangyu Zhao
Guoliang Bao
Hanwei Kong
Chao Ge
Fanglin Zhang
Tao Yu
Jinjun Li
Xianghuo He
Ming YaoState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 200032 Shanghai, China. myao@shsci.org.
Renji Hospital · CNShanghai Cancer Institute · CNShanghai Jiao Tong University · CNState Key Laboratory of Oncogene and Related Genes · CNShanghai Chest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGrowing evidence indicates that miR-200c is involved in carcinogenesis and tumor progression in non-small-cell lung cancer (NSCLC). However, its precise biological role remains largely elusive.

methodsThe functions of miR-200c and USP25 in migration/invasion and lung metastasis formation were determined by transwell and tail vein injection assays, respectively. The potential regulatory targets of miR-200c were determined by prediction tools, correlation with target protein expression, and luciferase reporter assay. The mRNA expression levels of miR-200c and USP25 were examined in NSCLC cell lines and patient specimens using quantitative reverse transcription-PCR. The protein expression levels of USP25 were examined in NSCLC cell lines and patient specimens using western blot and immunohistochemical staining.

resultsWe demonstrated that over-expression of miR-200c inhibited NSCLC cells migration, invasion, epithelial-mesenchymal transition (EMT) in vitro and lung metastasis formation in vivo. Further studies revealed that USP25 was a downstream target of miR-200c in NSCLC cells as miR-200c bound directly to the 3'-untranslated region of USP25, thus reducing both the messenger RNA and protein levels of USP25. Silencing of the USP25 gene recapitulated the effects of miR-200c over-expression. Clinical analysis indicated that miR-200c was negatively correlated with clinical stage, lymph node metastasis in NSCLC patients. Moreover, USP25 protein and mRNA level expressions were higher in NSCLC patients, compared to healthy control, and correlated with clinical stage and lymphatic node metastasis.

conclusionsThese findings indicate that miR-200c exerts tumor-suppressive effects for NSCLC through the suppression of USP25 expression and suggests a new therapeutic application of miR-200c in the treatment of NSCLC.

Indexed as

AgedAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansLung NeoplasmsLymphatic MetastasisMaleMiceMicroRNAsMiddle AgedNeoplasm InvasivenessMicroRNAsMIRN200 microRNA, humanUbiquitin ThiolesteraseUSP25 protein, human

Identifiers

PMID24997798
PMCPMC4105889
OpenAlexW2130747444

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.