Evidence map›Paper›PMID 41167420›Full record

ArticleJournal of advanced research2026

Ginsenoside Rg3 inhibits melanoma progression by inducing ferroptosis via the p53/SLC7A11/GPX4 pathway.

Anting Ma, Shunyao Zhu, Xiaowen Yao, Yusang Chen, Jingjing Yao, Mengdan Shen, Senlin Shi, Xi Han, Ting Zhang

Abstract read
In one paragraph

Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Antioxidants (Basel, Switzerland) · 2026
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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

9 authors.

Anting MaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 548 Binwen Road, Hangzhou, Zhejiang 310053, China.
Shunyao ZhuSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 548 Binwen Road, Hangzhou, Zhejiang 310053, China.
Xiaowen YaoSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 548 Binwen Road, Hangzhou, Zhejiang 310053, China.
Yusang ChenSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 548 Binwen Road, Hangzhou, Zhejiang 310053, China.
Jingjing YaoSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 548 Binwen Road, Hangzhou, Zhejiang 310053, China.
Mengdan ShenSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 548 Binwen Road, Hangzhou, Zhejiang 310053, China.
Senlin ShiSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 548 Binwen Road, Hangzhou, Zhejiang 310053, China.
Xi HanSchool of Medical Technology and Information Engineering, Zhejiang Chinese Medical University, Hangzhou 310053, China. Electronic address: 20241149@zcmu.edu.cn.
Ting ZhangSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, 548 Binwen Road, Hangzhou, Zhejiang 310053, China. Electronic address: zhangting55@zcmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionMelanoma represents an aggressive cutaneous malignancy with limited treatment options. Ginsenoside Rg3, an active component extracted from the roots of Panax ginseng, has been extensively demonstrated to possess significant anti-tumor efficacy, showing promising application potential in the treatment of various malignancies. However, the role of Rg3 in melanoma treatment and its related mechanisms have not been reported in detail. Thus, exploring and elucidating reliable molecular mechanisms is critical.

objectivesThis study aimed to investigate the therapeutic efficacy of ginsenoside Rg3 in melanoma and its underlying mechanisms.

methodsThis research investigated the mechanism of melanoma pathogenesis using a clinical cohort database and established a corresponding disease model. By integrating transcriptomic and metabolomic approaches, we systematically explored the intrinsic molecular mechanisms by which Rg3 regulated ferroptosis in melanoma. Then, immunohistochemistry (IHC), reverse transcription quantitative polymerase chain reaction (RT-qPCR), western blotting (WB), molecular docking (MD), and molecular dynamics simulation (MDS) were used for validation.

resultsThe database analysis revealed that melanoma was associated with the ferroptosis pathway. In vitro experiments showed that Rg3 inhibited the proliferation of melanoma cells. The functional annotation and enrichment analysis of differentially expressed genes and metabolites based on animal transcriptome and metabolome experiments showed that Rg3 exerted therapeutic effects by regulating the glutathione metabolism pathway and ferroptosis pathway. The detection based on the reagent kit revealed significant changes in ferroptosis-related biomarkers. IHC, RT-qPCR, and WB analyses confirmed the expression patterns of ferroptosis-associated mRNAs and proteins. MD and MDS confirmed stable binding between Rg3 and p53, SLC7A11, GPX4, and FTH1 proteins.

conclusionRg3 induced melanoma ferroptosis via the p53/SLC7A11/GPX4 pathway, offering therapeutic potential for melanoma.

Indexed as

FerroptosisGinsenosidesMelanomaTumor Suppressor Protein p53AnimalsCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceMolecular Docking SimulationSignal Transductionginsenoside Rg3GinsenosidesTumor Suppressor Protein p53FerroptosisGinsenoside Rg3Melanomap53/SLC7A11/GPX4

Identifiers

PMID41167420
PMCPMC13316401

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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.