Evidence map›Paper›PMID 28431583›Full record

ArticleJournal of experimental & clinical cancer research : CR2017

Overexpression of miR-584-5p inhibits proliferation and induces apoptosis by targeting WW domain-containing E3 ubiquitin protein ligase 1 in gastric cancer.

Qing Li, Zheng Li, Song Wei, Weizhi Wang, Zheng Chen, Lei Zhang, Liang Chen, Bowen Li, Guangli Sun, Jianghao Xu and 7 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
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  6. Insight into the Role of the miR-584 Family in Human Cancers.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Portrait of WWP1: the current state in human cancer.Frontiers in cell and developmental biology · 2024
    Review
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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

17 authors at 3 institutions in 2 countries.

Qing LiDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Zheng LiDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Song WeiDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Weizhi WangDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Zheng ChenDepartment of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Lei ZhangDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Liang ChenDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Bowen LiDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Guangli SunDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Jianghao XuDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Qiang LiDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Lu WangDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Zhipeng XuDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Yiwen XiaDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Diancai ZhangDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Hao XuDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China.
Zekuan XuDepartment of General Surgery, The First Affiliated Hospital of Nanjing Medical University, No.300, Guangzhou road, Nanjing, Jiangsu province, China. xuzekuan@njmu.edu.cn.
Jiangsu Province Hospital · CNNanjing Medical University · CNVanderbilt University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNAs are endogenously expressed, small non-coding RNAs that modulate gene expression by targeting specific mRNAs, resulting in translational repression or mRNA degradation. Although miR-584-5p has been reported to play a vital role in various malignancies, its role and the molecular mechanisms underlying the effects of miR-584-5p in gastric cancer (GC) remain to be clarified. In this study, we investigated the role of miR-584-5p in GC.

methodsThe expression of miR-584-5p and its specific target gene were determined in human GC specimens and cell lines by microRNA real-time polymerase chain reaction (RT-PCR), quantitative RT-PCR (qRT-PCR) and Western blot. The effects of miR-584-5p depletion or ectopic expression on GC proliferation were evaluated in vitro using CCK-8 proliferation assays, 5-ethynyl-2'-deoxyuridine (EdU) incorporation, colony formation assays and cell-cycle assays and the in vivo effects were investigated using a mouse tumorigenicity model. Cell apoptosis was evaluated by in vitro flow cytometric analysis, cell viability assays and in vivo TUNEL assays. Luciferase reporter assays were employed to identify interactions between miR-584-5p and its specific target gene.

resultsA series of in vitro and in vivo gain- and loss-of-function assays revealed that miR-584-5p inhibited GC cell proliferation, while apoptosis was induced. Luciferase reporter assays and Western blot analysis revealed WWP1 to be a direct target of miR-584-5p. The effects of miR-584-5p-mimic were rescued by WWP1 overexpression. In contrast, the effects of the miR-584-5p-inhibitor were impaired by WWP1-shRNA. Furthermore, miR-584-5p expression levels correlated negatively with WWP1 protein expression in GC tissues and GC cell lines. A series of investigations indicated that miR-584-5p promoted senescence and activated the TGFβ signaling pathway by downregulation of WWP1.

conclusionTaken together, these results suggest that downregulation of miR-584-5p contributes to tumor progression by downregulation of WWP1, thus, highlighting the potential of miR-584-5p as a therapeutic target for human GC.

Indexed as

Up-Regulation3' Untranslated RegionsAnimalsApoptosisCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMicroRNAsNeoplasm TransplantationSignal TransductionStomach Neoplasms3' Untranslated RegionsMicroRNAsMIRN584 microRNA, humanUbiquitin-Protein LigasesWWP1 protein, humanApoptosisCellular senescenceGastric cancermiR-584-5pProliferationTGFβ signaling pathwayWWP1

Identifiers

PMID28431583
PMCPMC5401563
OpenAlexW2606114225

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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.