Evidence map›Paper›PMID 35458126›Full record

ArticleNutrients2022

Ginsenoside Rh4 Suppresses Metastasis of Gastric Cancer via SIX1-Dependent TGF-β/Smad2/3 Signaling Pathway.

Hongbo Jiang, Pei Ma, Zhiguang Duan, Yannan Liu, Shihong Shen, Yu Mi, Daidi Fan

Abstract read
In one paragraph

Article in Nutrients, 2022. 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
–field-weighted citation impact
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.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Ginsenoside Rh4 Triggers Ferroptosis in Lung Cancer: TargetingInternational journal of molecular sciences · 2026
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Ginsenoside Rh7 affects β-catenin nuclear translocation by inhibitingInternational journal of medical sciences · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

7 authors.

Hongbo JiangShaanxi Key Laboratory of Degradable Biomedical Materials, Shaanxi R&D Center of Biomaterials, Fermentation Engineering, School of Chemical Engineering, Northwest University, Taibai North Road 229, Xi'an 710069, China.
Pei MaShaanxi Key Laboratory of Degradable Biomedical Materials, Shaanxi R&D Center of Biomaterials, Fermentation Engineering, School of Chemical Engineering, Northwest University, Taibai North Road 229, Xi'an 710069, China.
Zhiguang DuanShaanxi Key Laboratory of Degradable Biomedical Materials, Shaanxi R&D Center of Biomaterials, Fermentation Engineering, School of Chemical Engineering, Northwest University, Taibai North Road 229, Xi'an 710069, China.
Yannan LiuShaanxi Key Laboratory of Degradable Biomedical Materials, Shaanxi R&D Center of Biomaterials, Fermentation Engineering, School of Chemical Engineering, Northwest University, Taibai North Road 229, Xi'an 710069, China.
Shihong ShenShaanxi Key Laboratory of Degradable Biomedical Materials, Shaanxi R&D Center of Biomaterials, Fermentation Engineering, School of Chemical Engineering, Northwest University, Taibai North Road 229, Xi'an 710069, China.
Yu MiShaanxi Key Laboratory of Degradable Biomedical Materials, Shaanxi R&D Center of Biomaterials, Fermentation Engineering, School of Chemical Engineering, Northwest University, Taibai North Road 229, Xi'an 710069, China.ORCID 0000-0001-9360-4644
Daidi FanShaanxi Key Laboratory of Degradable Biomedical Materials, Shaanxi R&D Center of Biomaterials, Fermentation Engineering, School of Chemical Engineering, Northwest University, Taibai North Road 229, Xi'an 710069, China.

Funding

National Natural Sciences Foundation of China 21776227National Natural Sciences Foundation of China 22108224Natural Science Foundation of Shaanxi Province, China 2020JQ-570the National Key R&D Program of China 2021YFC2101000
6 · The paper itself

Abstract

Gastric cancer (GC) is the leading causes of cancer-related death worldwide. Surgery remains the cornerstone of gastric cancer treatment, and new strategies with adjuvant chemotherapy are currently gaining more and more acceptance. Ginsenoside Rh4 has excellent antitumor activity. Conversely, the mechanisms involved in treatment of GC are not completely understood. In this study, we certified that Rh4 showed strong anti-GC efficiency in vitro and in vivo. MTT and colony formation assays were performed to exhibit that Rh4 significantly inhibited cellular proliferation and colony formation. Results from the wound healing assay, transwell assays, and Western blotting indicated that Rh4 restrained GC cell migration and invasion by reversing epithelial-mesenchymal transition (EMT). Further validation by proteomic screening, co-treatment with disitertide, and SIX1 signal silencing revealed that SIX1, a target of Rh4, induced EMT by activating the TGF-β/Smad2/3 signaling pathway. In summary, our discoveries demonstrated the essential basis of the anti-GC metastatic effects of Rh4 via suppressing the SIX1-TGF-β/Smad2/3 signaling axis, which delivers a new idea for the clinical treatment of GC.

Indexed as

GinsenosidesStomach NeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHomeodomain ProteinsHumansProteomicsSignal TransductionSmad2 ProteinTransforming Growth Factor betaginsenoside Rh4GinsenosidesHomeodomain ProteinsSIX1 protein, humanSmad2 ProteinSMAD2 protein, humanTransforming Growth Factor betagastric cancerginsenoside Rh4SIX1TGF-β/Smad2/3 pathway

Identifiers

PMID35458126
PMCPMC9032069

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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.