Evidence map›Paper›PMID 33625675›Full record

ArticleJournal of physiology and biochemistry2021

Gastrin-17 induces gastric cancer cell epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway.

YaJie Li, Yan Zhao, Yi Li, XiaoYi Zhang, Chao Li, NiYa Long, XueShu Chen, LiYa Bao, JianJiang Zhou, Yuan Xie

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of physiology and biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Signaling pathways and therapeutic interventions in gastric cancer.Signal transduction and targeted therapy · 2022
    Review
  9. 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

10 authors at 1 institution in 1 country.

YaJie LiKey Laboratory of Endemic and Ethnic Diseases (Guizhou Medical University), Ministry of Education, Guizhou, China.
Yan ZhaoKey Laboratory of Endemic and Ethnic Diseases (Guizhou Medical University), Ministry of Education, Guizhou, China.
Yi LiKey Laboratory of Endemic and Ethnic Diseases (Guizhou Medical University), Ministry of Education, Guizhou, China.
XiaoYi ZhangKey Laboratory of Endemic and Ethnic Diseases (Guizhou Medical University), Ministry of Education, Guizhou, China.
Chao LiKey Laboratory of Endemic and Ethnic Diseases (Guizhou Medical University), Ministry of Education, Guizhou, China.
NiYa LongKey Laboratory of Endemic and Ethnic Diseases (Guizhou Medical University), Ministry of Education, Guizhou, China.
XueShu ChenKey Laboratory of Endemic and Ethnic Diseases (Guizhou Medical University), Ministry of Education, Guizhou, China.
LiYa BaoAffiliated Hospital, Guiyang Medical University, No. 9, Beijing Road, Guiyang, 550004, China.
JianJiang ZhouKey Laboratory of Endemic and Ethnic Diseases (Guizhou Medical University), Ministry of Education, Guizhou, China.
Yuan XieKey Laboratory of Endemic and Ethnic Diseases (Guizhou Medical University), Ministry of Education, Guizhou, China. xieyuan@gmc.edu.cn.ORCID http://orcid.org/0000-0001-9822-7374
Guiyang Medical University · CN

Funding

Guizhou Science and Technology Innovation Talent Team qiankehepingtairencai[2017]5652National Natural Science Foundation of China 31660031National Natural Science Foundation of China 31760328National Natural Science Foundation of China 31960028Project of Science and Technology of Guiyang ZhuKeHe[2017]30-4
6 · The paper itself

Abstract

Gastric cancer (GC) is one of the most common cancers, with most patients often succumbing to death as a result of tumor metastasis. Recent work has demonstrated that gastrin is closely associated with GC metastasis. However, the specific molecular mechanisms underlying this relationship remain to be unveiled. In this study, we assessed the impact of gastrin and the Wnt/β-catenin inhibitor XAV939 on the epithelial-mesenchymal transition (EMT) of the SGC-7901 and MKN45 GC cell lines, and we determined that gastrin-17 significantly decreased E-cadherin expression and upregulated the expression of Snail1 and N-cadherin in GC cells. In addition, gastrin 17 also significantly increased the expression of Wnt3α in a dose-dependent manner. Consistent with these results, gastrin-17 promoted GC cell invasion, proliferation, and migration in a dose-dependent fashion, and these effects were inhibited by XAV939. Together, these results indicated that gastrin-17 induced GC cell EMT, migration, and invasion via the Wnt/β-catenin signaling pathway, which suggests that this gastrin/Wnt/β-catenin signaling axis may represent a therapeutic target for the prevention of GC metastasis.

Indexed as

Cell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGastrinsHumansSnail Family Transcription FactorsStomach NeoplasmsWnt Signaling Pathwaygastrin 17GastrinsSnai1 protein, mouseSnail Family Transcription FactorsEpithelial-mesenchymal transitionGastric cancerGastrin-17MalignantWnt/β-catenin

Identifiers

PMID33625675
OpenAlexW3130306836

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.