Evidence map›Paper›PMID 30050309›Full record

ArticleOncoTargets and therapy2018

DcR3 induces proliferation, migration, invasion, and EMT in gastric cancer cells via the PI3K/AKT/GSK-3β/β-catenin signaling pathway.

Hua Ge, Chaojie Liang, Zhixia Li, Dali An, Shulin Ren, Chaosen Yue, Jixiang Wu

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.0field-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

26 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  6. Research Progress of DcR3 in the Diagnosis and Treatment of Sepsis.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
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  10. Frontiers in pharmacology · 2022
    Article
  11. Article
  12. Review
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  16. Review
  17. S100A16 Regulates HeLa Cell through the Phosphatidylinositol 3 Kinase (PI3K)/AKT Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  18. Article
  19. Article
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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

7 authors at 1 institution in 1 country.

Hua GeDepartment of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China, trwujixiang2017@126.com.
Chaojie LiangDepartment of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China, trwujixiang2017@126.com.
Zhixia LiDepartment of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China, trwujixiang2017@126.com.
Dali AnDepartment of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China, trwujixiang2017@126.com.
Shulin RenDepartment of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China, trwujixiang2017@126.com.
Chaosen YueDepartment of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China, trwujixiang2017@126.com.
Jixiang WuDepartment of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China, trwujixiang2017@126.com.
Beijing Tongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDecoy receptor 3 (DcR3) has been reported to be overexpressed in a wide variety of malignancies and is correlated with tumorigenesis and progression. In gastric cancer (GC), DcR3 overexpression is associated with lymph node and distant metastasis, as well as poor prognosis. However, the functional role of DcR3 expression in GC remains elusive. PURPOSE: The aim of this study is to elucidate the direct role of DcR3 in regulating GC progression and metastasis and identify the potential mechanism.

methodsDcR3 expression was stably knocked down in HGC27 and MKN28 cells by transfecting the cells with DcR3 shRNA using lentiviral vector system. After the knockdown of DcR3 was confirmed, cell proliferation, colony formation, cell cycle distribution, apoptosis, cell invasion and migration were assessed in vitro. In addition, Western blot analysis was performed to evaluate the expression of downstream mediators of DcR3. Comparisons between multiple groups were performed using one-way analysis of variance (ANOVA) or unpaired Student's

resultsOur findings demonstrate that DcR3 induces proliferation, migration, invasion, and promotes epithelial-mesenchymal transition (EMT) of GC cells. In addition, DcR3 increases the expression levels of several components of the PI3K/AKT/GSK-3β/β-catenin signaling pathway, such as p-AKT, GSK-3β, p-GSK-3β and β-catenin. Additionally, DcR3 also enhances the expression of N-cadherin and Vimentin and decreases the expression of E-cadherin.

conclusionIn summary, the findings of this study indicate that during GC progression, DcR3 plays a key role in cell proliferation and invasion via the PI3K/AKT/GSK-3β/β-catenin signaling pathway. Thus, targeting DcR3 might be a potential therapeutic approach for the treatment of GC.

Indexed as

DcR3epithelial-mesenchymal transitiongastric cancermetastasis

Identifiers

PMID30050309
PMCPMC6056154
OpenAlexW2883315636

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.