Evidence map›Paper›PMID 25636908›Full record

ArticleJournal of experimental & clinical cancer research : CR2015

MiR-203 down-regulates Rap1A and suppresses cell proliferation, adhesion and invasion in prostate cancer.

Jun Xiang, Cuidong Bian, Hao Wang, Shengsong Huang, Denglong Wu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  5. pH-sensing GPR68 inhibits vascular smooth muscle cell proliferation through Rap1A.American journal of physiology. Heart and circulatory physiology · 2024
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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

5 authors at 3 institutions in 1 country.

Jun XiangDepartment of Urology, Tongji Hospital, Tongji University School of Medicine, NO 389 Xinchun road, Shanghai, 200065, China. zhuxufifa2007@163.com.
Cuidong BianDepartment of Urology, Tongji Hospital, Tongji University School of Medicine, NO 389 Xinchun road, Shanghai, 200065, China. 071101023@fudan.edu.cn.
Hao WangThe Experimental Center of Basic Medical, Shanghai Medical College, Fudan University, Shanghai, 200032, China. wh91351@126.com.
Shengsong HuangDepartment of Urology, Tongji Hospital, Tongji University School of Medicine, NO 389 Xinchun road, Shanghai, 200065, China. YanWangArmy@163.com.
Denglong WuDepartment of Urology, Tongji Hospital, Tongji University School of Medicine, NO 389 Xinchun road, Shanghai, 200065, China. wudeng123long@163.com.
Tongji Hospital · CNTongji University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveEvidence supports an important role for miR-203 in the regulation of the proliferation, migration and invasion of prostate cancer (PCa) cells. However, the exact mechanisms of miR-203 in PCa are not entirely clear.

methodsWe examined the expression of miR-203 in prostate cancer tissues, adjacent normal tissues, PCa cell lines and normal prostate epithelial cells by qRT-PCR. Then, the effects of miR-203 or Rap1A on proliferation, adhesion and invasion of PCa cells were assayed using CKK-8, adhesion analysis, and transwell invasion assays. Luciferase reporter assay was performed to assess miR-203 binding to Rap1A mRNA. Tumor growth was assessed by subcutaneous inoculation of cells into BALB/c nude mice.

resultsHere, we confirmed that the expression of miR-203 was significantly downregulated in prostate cancer specimens compared with matched adjacent normal prostate specimens. Mechanistic dissection revealed that miR-203 mediated cell proliferation, adhesion and invasion in vitro, and tumor growth in vivo, as evidenced by reduced RAC1, p-PAK1, and p-MEK1 expression. In addition, we identified Rap1A as a direct target suppressed by miR-203, and there was an inverse relationship between the expression of miR-203 and Rap1A in PCa. Knockdown of Rap1A phenocopied the effects of miR-203 on PCa cell growth and invasion. Furthermore, Rap1A over-expression in PCa cells partially reversed the effects of miR-203-expression on cell adhesion and invasion.

conclusionsThese findings provide further evidence that a crucial role for miR-203 in inhibiting metastasis of PCa through the suppression of Rap1A expression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBase SequenceBinding SitesCell AdhesionCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalDown-RegulationGene ExpressionGene Knockdown TechniquesGenes, ReporterHumansMaleMicroRNAsMicroRNAsMIRN203 microRNA, humanrap1 GTP-Binding ProteinsRNA, Messenger

Identifiers

PMID25636908
PMCPMC4321708
OpenAlexW2135536986

What OpenQuestion holds

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LicenceCC BY
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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.