Evidence map›Paper›PMID 30542715›Full record

ArticleOncology reports2018

Inhibition of miR‑194 suppresses the Wnt/β‑catenin signalling pathway in gastric cancer.

Yin Peng, Xiaojing Zhang, Huijuan Lin, Shiqi Deng, Yong Huang, Ying Qin, Xianling Feng, Ruibin Yan, Yanqiu Zhao, Yulan Cheng and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 41% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

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  11. MiR-194 promotes hepatocellular carcinoma through negative regulation of CADM1.International journal of clinical and experimental pathology · 2020
    Article
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

20 authors at 9 institutions in 2 countries.

Yin PengGuangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pathology, The Shenzhen University School of Medicine, Shenzhen, Guangdong 518060, P.R. China.
Xiaojing ZhangGuangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pathology, The Shenzhen University School of Medicine, Shenzhen, Guangdong 518060, P.R. China.
Huijuan LinDepartment of Pathology and Pathophysiology, The Guangzhou Medical University, Guangzhou, Guangdong 510000, P.R. China.
Shiqi DengGuangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pathology, The Shenzhen University School of Medicine, Shenzhen, Guangdong 518060, P.R. China.
Yong HuangGuangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pathology, The Shenzhen University School of Medicine, Shenzhen, Guangdong 518060, P.R. China.
Ying QinDepartment of Gastrointestinal Surgery, Shenzhen Second People's Hospital, Shenzhen, Guangdong 518000, P.R. China.
Xianling FengGuangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pathology, The Shenzhen University School of Medicine, Shenzhen, Guangdong 518060, P.R. China.
Ruibin YanLaboratory of Chemical Genomics, The Shenzhen Graduate School of Peking University, Shenzhen, Guangdong 518055, P.R. China.
Yanqiu ZhaoLaboratory of Chemical Genomics, The Shenzhen Graduate School of Peking University, Shenzhen, Guangdong 518055, P.R. China.
Yulan ChengDepartment of Medicine/GI Division, The Johns Hopkins University School of Medicine and Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD 21287, USA.
Yanjie WeiCenter for High Performance Computing, Shenzhen Institutes of Advanced Technology, Shenzhen, Guangdong 518000, P.R. China.
Jian WangDepartment of Pathology and Pathophysiology, The Guangzhou Medical University, Guangzhou, Guangdong 510000, P.R. China.
Wangchun ChenGuangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pathology, The Shenzhen University School of Medicine, Shenzhen, Guangdong 518060, P.R. China.
Xinmin FanGuangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pathology, The Shenzhen University School of Medicine, Shenzhen, Guangdong 518060, P.R. China.
Hassan AshktorabDepartment of Medicine and Cancer Center, Howard University, College of Medicine, Washington, DC 20060, USA.
Duane SmootDepartment of Medicine, Meharry Medical Center, Nashville, TN 37208, USA.
Stephen J MeltzerDepartment of Medicine/GI Division, The Johns Hopkins University School of Medicine and Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD 21287, USA.
Song LiLaboratory of Chemical Genomics, The Shenzhen Graduate School of Peking University, Shenzhen, Guangdong 518055, P.R. China.
Zhong ZhangDepartment of Pathology, College of Basic Medical Sciences, Shenyang Medical College, Shenyang, Liaoning 110034, P.R. China.
Zhe JinGuangdong Key Laboratory for Genome Stability & Disease Prevention, Department of Pathology, The Shenzhen University School of Medicine, Shenzhen, Guangdong 518060, P.R. China.
Shenzhen University · CNPeking University · CNGuangzhou Medical University · CNJohns Hopkins University · USHoward University · USMeharry Medical College · USShenyang Medical College · CNShenzhen Institutes of Advanced Technology · CNShenzhen Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A mounting body of evidence has revealed that microRNAs (miRs) serve pivotal roles in various developmental processes, and in tumourigenesis, by binding to target genes and subsequently regulating gene expression. Continued activation of the Wnt/β‑catenin signalling is positively associated with human malignancy. In addition, miR‑194 dysregulation has been implicated in gastric cancer (GC); however, the molecular mechanisms underlying the effects of miR‑194 on GC carcinogenesis remain to be elucidated. The present study demonstrated that miR‑194 was upregulated in GC tissues and SUFU negative regulator of Ηedgehog signaling (SUFU) was downregulated in GC cell lines. Subsequently, inhibition of miR‑194 attenuated nuclear accumulation of β‑catenin, which consequently blocked Wnt/β‑catenin signalling. In addition, the cytoplasmic translocation of β‑catenin induced by miR‑194 inhibition was mediated by SUFU. Furthermore, genes associated with the Wnt/β‑catenin signalling pathway were revealed to be downregulated following inhibition of the Wnt signalling pathway by miR‑194 suppression. Finally, the results indicated that cell apoptosis was markedly increased in response to miR‑194 inhibition, strongly suggesting the carcinogenic effects of miR‑194 in GC. Taken together, these findings demonstrated that miR‑194 may promote gastric carcinogenesis through activation of the Wnt/β‑catenin signalling pathway, making it a potential therapeutic target for GC.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAged, 80 and overApoptosisCarcinogenesisCell Line, TumorCell ProliferationDown-RegulationFemaleHumansMaleMicroRNAsMiddle AgedRepressor ProteinsStomachMicroRNAsMIRN194 microRNA, humanRepressor ProteinsSUFU protein, humanTumor Suppressor Proteins

Identifiers

PMID30542715
PMCPMC6196585
OpenAlexW2897014457

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.