Evidence map›Paper›PMID 37092860›Full record

ArticleActa biochimica et biophysica Sinica2023

Ginsenoside Rh3 induces pyroptosis and ferroptosis through the Stat3/p53/NRF2 axis in colorectal cancer cells.

Yingchao Wu, Dajin Pi, Shuyao Zhou, Zhongjia Yi, Yangyang Dong, Wuhong Wang, Huan Ye, Yiliu Chen, Qian Zuo, Mingzi Ouyang

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
13.2field-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

95 citing papers in PubMed, 86 citations in OpenAlex.

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  7. Mechanism-centered target discovery across glomerulonephritis phenotypes: an integrative multi-omics study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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35 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Yingchao WuSchool of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China.
Dajin PiSchool of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China.
Shuyao ZhouCollege of Forestry and Landscape Architecture, South China Agricultural University, Guangzhou 510642, China.
Zhongjia YiSchool of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China.
Yangyang DongGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, Guangdong Pharmaceutical University, Guangzhou 510006, China.
Wuhong WangSchool of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China.
Huan YeSchool of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China.
Yiliu ChenSchool of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China.
Qian ZuoMOE Key Laboratory of Tumor Molecular Biology and Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes, Institute of Life and Health Engineering, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
Mingzi OuyangSchool of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China.
Jinan University · CNGuangdong Pharmaceutical University · CNSouth China Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ginsenoside Rh3 (GRh3) is a seminatural product obtained by chemical processing after isolation from Chinese herbal medicine that has strong antitumor activity against human tumors. However, its antitumor role remains to be elucidated. The aim of this study is to explore the mechanisms underlying the tumor suppressive activity of GRh3 from the perspective of pyroptosis and ferroptosis. GRh3 eliminates colorectal cancer (CRC) cells by activating gasdermin D (GSDMD)-dependent pyroptosis and suppressing solute carrier family 7 member 11 (SLC7A11), resulting in ferroptosis activation through the Stat3/p53/NRF2 axis. GRh3 suppresses nuclear factor erythroid 2-related factor 2 (NRF2) entry into the nucleus, leading to the decrease of heme oxygenase 1 (HO-1) expression, which in turn promotes NOD-like receptor thermal protein domain associated protein 3 (NLRP3) and caspase-1 expression. Finally, caspase-1 activates GSDMD-dependent pyroptosis. Furthermore, GRh3 prevents NRF2 from entering the nucleus, which suppresses SLC7A11, causing the depletion of glutathione (GSH) and accumulation of iron, lipid reactive oxygen species (ROS) and malondialdehyde (MDA), and eventually leading to ferroptosis in CRC cells. In addition, GRh3 effectively inhibits the proliferation of CRC cells

Indexed as

Colorectal NeoplasmsFerroptosisAnimalsCaspase 1GinsenosidesGlutathioneHumansMiceMice, NudeNF-E2-Related Factor 2PyroptosisSTAT3 Transcription FactorTumor Suppressor Protein p53Caspase 1ginsenoside Rh3GinsenosidesGlutathioneNF-E2-Related Factor 2STAT3 protein, humanSTAT3 Transcription FactorTumor Suppressor Protein p53colorectal cancerferroptosisginsenoside Rh3pyroptosisStat3/p53/NRF2 axis

Identifiers

PMID37092860
PMCPMC10195137
OpenAlexW4363625498

What OpenQuestion holds

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LicenceCC BY
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.