Evidence map›Paper›PMID 38163861›Full record

ArticleBiology direct2024

GPR137 inactivates Hippo signaling to promote gastric cancer cell malignancy.

Lin Li, Jinlong Tang, Bin Cao, Qiang Xu, Shouying Xu, Chao Lin, Chao Tang

Open access · goldAbstract read
In one paragraph

Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
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  9. Review
  10. GPR137-RAB8A activation promotes ovarian cancer development via the Hedgehog pathway.Journal of experimental & clinical cancer research : CR · 2025
    Article
  11. Article
  12. Review
  13. Cell signaling inFrontiers in cellular and infection microbiology · 2025
    Review
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

7 authors at 3 institutions in 1 country.

Lin Li *National Clinical Research Center for Child Health, The Children's Hospital, Zhejiang University School of Medicine, No. 3333, Binsheng Road, Hangzhou, 310052, People's Republic of China.
Jinlong Tang *Department of Pathology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310005, People's Republic of China.
Bin Cao *Zhejiang Provincial Center for Disease Control and Prevention, Hangzhou, People's Republic of China.
Qiang XuNational Clinical Research Center for Child Health, The Children's Hospital, Zhejiang University School of Medicine, No. 3333, Binsheng Road, Hangzhou, 310052, People's Republic of China.
Shouying XuNational Clinical Research Center for Child Health, The Children's Hospital, Zhejiang University School of Medicine, No. 3333, Binsheng Road, Hangzhou, 310052, People's Republic of China.
Chao LinDepartment of Neurosurgery, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, 310052, People's Republic of China.
Chao TangNational Clinical Research Center for Child Health, The Children's Hospital, Zhejiang University School of Medicine, No. 3333, Binsheng Road, Hangzhou, 310052, People's Republic of China. chtang@zju.edu.cn.
Children's Hospital of Zhejiang University · CNSecond Affiliated Hospital of Zhejiang University · CNZhejiang Center for Disease Control and Prevention · CN

Funding

National Natural Science Foundation of China 31801207
6 · The paper itself

Abstract

As the fifth most common cancer in the world, gastric cancer (GC) ranks as the third major cause of cancer-related death globally. Although surgical resection and chemotherapy still remains the mainstay of potentially curative treatment for GC, chemotherapy resistance and adverse side effects limit their clinical applications. Thus, further investigation of the mechanisms of carcinogenesis in GC and discovery of novel biomarkers is of great concern. We herein report that the elevated expression of GPR137 is correlated with GC. Overexpression of GPR137 potentiates human gastric cancer AGS cell malignancy, including proliferation, migration, invasion, colony formation and xenograft growth in nude mice in vivo, whereas knockout of GPR137 by CRISPR/Cas9 gene editing exerts the opposite effects. Mechanistically, GPR137 could bind to MST, the upstream kinases in Hippo pathway, which disrupts the association of MST with LATS, subsequently activating the transcriptional co-activators, YAP and TAZ, and thereby triggering the target transcription and the alterations in GC cell biological actions consequently. Therefore, our findings may provide with the evidence of developing a potentially novel treatment method with specific target for GC.

Indexed as

Hippo Signaling PathwayStomach NeoplasmsAnimalsCell Line, TumorCell ProliferationHumansMiceMice, NudeProtein Serine-Threonine KinasesSignal TransductionTranscription FactorsProtein Serine-Threonine KinasesTranscription FactorsGastric cancerGPR137HippoMST

Identifiers

PMID38163861
PMCPMC10759669
OpenAlexW4390498991

What OpenQuestion holds

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LicenceCC BY
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.