Evidence map›Paper›PMID 25743273›Full record

ArticleMolecular cancer2015

Targeting of YAP1 by microRNA-15a and microRNA-16-1 exerts tumor suppressor function in gastric adenocarcinoma.

Wei Kang, Joanna H M Tong, Raymond W M Lung, Yujuan Dong, Junhong Zhao, Qiaoyi Liang, Li Zhang, Yi Pan, Weiqin Yang, Jesse C S Pang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
7.0field-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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

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  13. The Hippo signaling pathway in gastric cancer.Acta biochimica et biophysica Sinica · 2023
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21 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

13 authors at 2 institutions in 1 country.

Wei KangDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. weikang@cuhk.edu.hk.
Joanna H M TongDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. jtong@cuhk.edu.hk.
Raymond W M LungDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. Raymond_lung@cuhk.edu.hk.
Yujuan DongInstitute of Digestive Disease, Partner State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. celia.yj.dong@gmail.com.
Junhong ZhaoInstitute of Digestive Disease, Partner State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. zhaojh_gz@163.com.
Qiaoyi LiangInstitute of Digestive Disease, Partner State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. JessieQY@cuhk.edu.hk.
Li ZhangDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. yblhzl@hotmail.com.
Yi PanDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. panyi@cuhk.edu.hk.
Weiqin YangSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, PR China. weiqinyang1021@cuhk.edu.hk.
Jesse C S PangDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. jessepang@cuhk.edu.hk.
Alfred S L ChengInstitute of Digestive Disease, Partner State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. alfredcheng@cuhk.edu.hk.
Jun YuInstitute of Digestive Disease, Partner State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. junyu@cuhk.edu.hk.
Ka Fai ToDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, SAR, PR China. kfto@cuhk.edu.hk.
Chinese University of Hong Kong · CNPrince of Wales Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNAs (miRNAs) have been reported to play an important role in tumorigenesis. In this study, the role of miR-15a and miR-16-1 in gastric adenocarcinoma (GAC) was investigated.

methodsThe expression of miR-15a and miR-16-1 in cell lines and primary tumors was examined by miRNA qRT-PCR. Proliferative assays, colony formation, cell invasion and migration, flow cytometry analysis and in vivo study were performed by ectopic expression of miR-15a and miR-16-1. The putative target genes of miR-15a and miR-16-1 were explored by TargetScan and further validated.

resultsWe found that miR-15a and miR-16-1 were down-regulated in GAC cell lines and primary tumor samples compared with normal gastric epithelium. Functional study demonstrated that ectopic expression of miR-15a and miR-16-1 suppressed cell proliferation, monolayer colony formation, invasion and migration, and xenograft formation in vivo. In addition, miR-15a and miR-16-1 induced G0/G1 cell cycle arrest which was further confirmed by Western blot and qRT-PCR of related cell cycle regulators. YAP1 was confirmed to be a functional target of miR-15a and miR-16-1 in GAC. YAP1 re-expression partly abrogated the inhibitory effect of miR-15a and miR-16-1 in GAC cells. In clinical samples, YAP1 protein expression shows negative correlation with miR-15a and miR-16-1 expression.

conclusionIn conclusion, targeting YAP1 by tumor suppressor miRNA miR-15a and miR-16-1 plays inhibitory effect and this might have a therapeutic potential in GAC.

Indexed as

Adaptor Proteins, Signal TransducingAdenocarcinomaAnimalsCell Line, TumorCell MovementCell ProliferationDown-RegulationG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansMiceMice, Inbred BALB CMice, NudeMicroRNAsPhosphoproteinsAdaptor Proteins, Signal TransducingMicroRNAsMIRN15 microRNA, humanMIRN16 microRNA, humanPhosphoproteinsTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID25743273
PMCPMC4342823
OpenAlexW2106382473

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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.