Evidence map›Paper›PMID 31933934›Full record

ArticleInternational journal of clinical and experimental pathology2019

Gpx3 prevents migration and invasion in gastric cancer by targeting NFкB/Wnt5a/JNK signaling.

Meijuan Cai, Yinhe Sikong, Qing Wang, Shuzhen Zhu, Fei Pang, Xiangdan Cui

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

38 citing papers in PubMed, 33 citations in OpenAlex.

  1. Role and Mechanism ofInternational journal of molecular sciences · 2026
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  10. Glutathione-Dependent Pathways in Cancer Cells.International journal of molecular sciences · 2024
    Review
  11. Advances in the role of GPX3 in ovarian cancer (Review).International journal of oncology · 2024
    Article
  12. Article
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  19. Prognostic value and immunological roles of GPX3 in gastric cancer.International journal of medical sciences · 2023
    Article
  20. 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

6 authors at 1 institution in 1 country.

Meijuan CaiDepartment of Clinical Laboratory, Qilu Hospital of Shandong University Qingdao, P. R. China.
Yinhe SikongDepartment of Gastroenterology, Qilu Hospital of Shandong University Qingdao, P. R. China.
Qing WangDepartment of Gastroenterology, Qilu Hospital of Shandong University Qingdao, P. R. China.
Shuzhen ZhuDepartment of Clinical Laboratory, Qilu Hospital of Shandong University Qingdao, P. R. China.
Fei PangDepartment of Gastroenterology, Qilu Hospital of Shandong University Qingdao, P. R. China.
Xiangdan CuiDepartment of Gastroenterology, Qilu Hospital of Shandong University Qingdao, P. R. China.
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMetastasis is the hallmark of gastric cancer (GC) and is the most widely recognized reason for GC-related deaths. However, the underlying mechanism of GC metastasis remains unknown. Herein we sought to investigate the biologic function of Gpx3 in gastric tumor metastasis and the underlying mechanism.

methodsCell migration and invasion was determined with Transwell chamber assay. Western blotting was used to determine protein expression levels of Gpx3, EMT markers and Wnt signaling related molecules.

resultsGpx3 expression was lower in GC patients and GC cell lines when compared with normal tissues and cells. Further studies showed that overexpression of Gpx3 was able to inhibit GC cell migration and invasion whereas Gpx3 knockdown promoted cell migration and invasion. Furthermore, AGS cells overexpressing Gpx3 showed lower metastatic potential when compared with the parental cells. Gpx3 was also found to regulate the expression of EMT markers. Mechanistic study showed that Gpx3 selectively inhibited Wnt/JNK signaling pathway over canonical Wnt/β-catenin pathway. The data revealed that blockade of NFкB and JNK signaling pathway abolished siGpx3-induced cell migration and invasion.

conclusionsTaken together, we identify Gpx3 as a suppressor of GC metastasis. Above results provide the rationale that regulation of Gpx3 serves as a potential therapeutic option for GC.

Indexed as

GCGpx3metastasisWnt

Identifiers

PMID31933934
PMCPMC6947061
OpenAlexW3026790418

What OpenQuestion holds

Textmetadata
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.