Evidence map›Paper›PMID 35079445›Full record

ArticleJournal of gastric cancer2021

Vitexin Inhibits Gastric Cancer Growth and Metastasis through HMGB1-mediated Inactivation of the PI3K/AKT/mTOR/HIF-1α Signaling Pathway.

Peng Zhou, Zi-Han Zheng, Tao Wan, Jie Wu, Chuan-Wen Liao, Xue-Jun Sun

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Journal of gastric cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  8. Review
  9. Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer Functions.International journal of molecular sciences · 2025
    Review
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  19. Targeting PI3K/AKT/mTOR and MAPK Signaling Pathways in Gastric Cancer.International journal of molecular sciences · 2024
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Peng ZhouDepartment of General Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.
Zi-Han ZhengDepartment of Gastrointestinal Surgery, Jiangxi Provincial People's Hospital, Nanchang, People's Republic of China.
Tao WanDepartment of Gastrointestinal Surgery, Jiangxi Provincial People's Hospital, Nanchang, People's Republic of China.
Jie WuDepartment of Gastrointestinal Surgery, Jiangxi Provincial People's Hospital, Nanchang, People's Republic of China.
Chuan-Wen LiaoDepartment of Gastrointestinal Surgery, Jiangxi Provincial People's Hospital, Nanchang, People's Republic of China.
Xue-Jun SunDepartment of General Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.
Jiangxi Provincial People's Hospital · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeGastric cancer (GC) has high morbidity and mortality and is a serious threat to public health. The flavonoid compound vitexin is known to exhibit anti-tumor activity. In this study, we explored the therapeutic potential of vitexin in GC and its underlying mechanism. MATERIALS AND

methodsThe viability, migration, and invasion of GC cells were determined using MTT, scratch wound healing, and transwell assays, respectively. Target molecule expression was determined by western blotting. Tumor growth and liver metastasis were evaluated in vivo using nude mice. Protein expression in the tumor tissues was examined by immunohistochemistry.

resultsVitexin inhibited GC cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT) in a dose-dependent manner. Vitexin treatment led to the inactivation of phosphatidylinositol-3-kinase (PI3K)/AKT/hypoxia-inducible factor-1α (HIF-1α) pathway by repressing

conclusionsVitexin inhibited the malignant progression of GC in vitro and in vivo by suppressing HMGB1-mediated activation of PI3K/Akt/HIF-1α signaling pathway. Thus, vitexin may serve as a promising therapeutic agent for the treatment of GC.

Indexed as

Epithelial-Mesenchymal transitionGastric cancerHypoxiaPhosphatidylinositolsVitexin

Identifiers

PMID35079445
PMCPMC8753280
OpenAlexW4205417452

What OpenQuestion holds

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LicenceCC BY-NC
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.