Evidence map›Paper›PMID 37397926›Full record

ArticleToxicology research2023

Celastrol inhibits gastric cancer cell proliferation, migration, and invasion via the FOXA1/CLDN4 axis.

Wei Peng, Lin Chen, Jie Liu

Open access · greenAbstract read
In one paragraph

Article in Toxicology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
12.7field-weighted citation impact, top 1% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  16. Effects of dietary NDF/NFC ratios onFrontiers in veterinary science · 2025
    Article
  17. Review
  18. The therapeutic potential ofTurkish journal of biology = Turk biyoloji dergisi · 2025
    Article
  19. Review
  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

3 authors at 2 institutions in 1 country.

Wei PengChangsha Social Work College, Changsha 410018, Hunan Province, China.
Lin ChenDepartment of Internal Medicine, The First Affiliated Hospital of Changsha Medical College, Changsha 410219, Hunan Province, China.
Jie LiuChangsha Social Work College, Changsha 410018, Hunan Province, China.
Changsha University · CNThe First Hospital of Changsha · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Celastrol is a biologically active compound with potent anti-tumor properties. However, the mechanism of action of celastrol in gastric cancer (GC) has not been fully elucidated. Methods: To explore the specific mechanism of the effect of celastrol on GC cells. GC cells were transfected with forkhead box A1 (FOXA1) or claudin 4 (CLDN4), or short hairpin RNA targeting FOXA1. The expressions of FOXA1 and CLDN4 in GC cells were determined by quantitative reverse transcription PCR and Western blot. GC cell proliferation, migration, and invasion were measured by MTT assay and Transwell assay, respectively. The interaction between CLDN4 and FOXA1 was examined by luciferase reporter assay. Resluts: CLDN4 and FOXA1 were upregulated in GC cells. Celastrol prevented the proliferation, migration, and invasion of GC cells by downregulating FOXA1 expression. Overexpression of FOXA1 or CLDN4 accelerated GC progression. CLDN4 overexpression also induced the activation of the expressions of phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway. FOXA1 enhanced the transcription of CLDN4. Conclusion: Celastrol regulated GC progression via targeting the FOXA1/CLDN4 axis to impede the PI3K/AKT pathway. Our study proposed a new mechanism of how celastrol inhibited tumorigenesis in GC, which provided evidence for the potential use of celastrol for anti-GC treatment.

Indexed as

celastrolCLDN4FOXA1gastric cancerPI3K/AKT pathway

Identifiers

PMID37397926
PMCPMC10311132
OpenAlexW4366686327

What OpenQuestion holds

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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.