Evidence map›Paper›PMID 31827075›Full record

ArticleCell death & disease2019

CLDN6 promotes tumor progression through the YAP1-snail1 axis in gastric cancer.

Site Yu, Yeqian Zhang, Qing Li, Zizhen Zhang, Gang Zhao, Jia Xu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
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  8. Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025
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  13. Claudins in Cancer: A Current and Future Therapeutic Target.International journal of molecular sciences · 2024
    Review
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  15. Article
  16. Article
  17. Review
  18. 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

6 authors at 2 institutions in 1 country.

Site YuDepartment of General Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160, Pujian Road, Shanghai, 200127, P.R. China.ORCID http://orcid.org/0000-0002-7630-3417
Yeqian ZhangDepartment of General Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160, Pujian Road, Shanghai, 200127, P.R. China.
Qing LiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, P.R. China.
Zizhen ZhangDepartment of General Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160, Pujian Road, Shanghai, 200127, P.R. China.
Gang ZhaoDepartment of General Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160, Pujian Road, Shanghai, 200127, P.R. China. zhaogang74313@aliyun.com.ORCID http://orcid.org/0000-0002-9999-9402
Jia XuDepartment of General Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, No. 160, Pujian Road, Shanghai, 200127, P.R. China. xujia78520@126.com.
Shanghai Jiao Tong University · CNRenji Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) No.31872740
6 · The paper itself

Abstract

Claudin6 (CLDN6), a member of the tight junction family, is a molecule involved in intercellular adhesion, acting as a physical barrier that prevents solutes and water from freely passing through the extracellular space. CLDN6 has important biological functions, and its abnormal expression is associated with Hepatitis C infection. However, there is limited research regarding its role in gastric cancer. In this study, we found that the expression of CLDN6 mRNA and protein was upregulated in gastric cancer cell lines and tissues, which indicated poor prognosis. Both in vitro and in vivo experiments showed that abnormal CLDN6 expression was associated with enhanced proliferation and invasion abilities of gastric cancer. CLDN6 reduced the phosphorylation of LATS1/2 and YAP1 by interacting with LATS1/2 in the Hippo signaling pathway. Thus, CLDN6 affected the entry of YAP1 into the nucleus, causing changes in downstream target genes. Moreover, YAP1 interacted with snail1 to affect the process of EMT and enhanced the invasive ability of GC cells. Collectively, CLDN6 promoted the proliferation and invasive ability of gastric cancer by affecting YAP1 and YAP1-snail1 axis.

Indexed as

Adaptor Proteins, Signal TransducingAgedCell Line, TumorCell ProliferationClaudinsDisease-Free SurvivalDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedPhosphorylationProtein Serine-Threonine KinasesSignal TransductionSnail Family Transcription FactorsAdaptor Proteins, Signal Transducingclaudin 6ClaudinsLATS1 protein, humanProtein Serine-Threonine KinasesSNAI1 protein, humanSnail Family Transcription FactorsTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID31827075
PMCPMC6906326
OpenAlexW2994864594

What OpenQuestion holds

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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.