ArticlePhytotherapy research : PTR2019
Ginseng metabolite protopanaxadiol interferes with lipid metabolism and induces endoplasmic reticulum stress and p53 activation to promote cancer cell death.
Article in Phytotherapy research : PTR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- A review of pharmacological properties and pharmacokinetic of 20(S)-protopanaxadiol.Journal of ginseng research · 2026Review
- Bioactive Constituents of Ginseng in Cancer Therapy: Molecular Mechanisms, Translational Potential, and Advanced Delivery Strategies.International journal of biological sciences · 2026Review
- Lipid Metabolism Reprogramming in Cancer: Insights into Tumor Cells and Immune Cells Within the Tumor Microenvironment.Biomedicines · 2025Review
- Targeting lipid reprogramming in the tumor microenvironment by traditional Chinese medicines as a potential cancer treatment.Heliyon · 2024Review
- A Novel Lipid Metabolism and Endoplasmic Reticulum Stress-Related Risk Model for Predicting Immune Infiltration and Prognosis in Colorectal Cancer.International journal of molecular sciences · 2023Article
- Protopanaxadiol ameliorates palmitate-induced lipotoxicity and pancreatic β-cell dysfunction in INS-1 cells.Journal of ginseng research · 2023Article
- Signaling pathways in cancer metabolism: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Lipid metabolic reprogramming by traditional Chinese medicine and its role in effective cancer therapy.Journal of Cancer · 2023Review
- Bioconversion variation of ginsenoside CK mediated by human gut microbiota from healthy volunteers and colorectal cancer patients.Chinese medicine · 2021Article
- Tannic acid inhibits lipid metabolism and induce ROS in prostate cancer cells.Scientific reports · 2020Article
- Ginseng metabolite Protopanaxadiol induces Sestrin2 expression and AMPK activation through GCN2 and PERK.Cell death & disease · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Protopanaxadiol (PPD), a ginseng metabolite generated by the gut bacteria, was shown to induce colorectal cancer cell death and enhance the anticancer effect of chemotherapeutic agent 5-FU. However, the mechanism by which PPD promotes cancer cell death is not clear. In this manuscript, we showed that PPD activated p53 and endoplasmic reticulum (ER) stress and induced expression of BH3-only proteins Puma and Noxa to promote cell death. Induction of Puma by PPD was p53-dependent, whereas induction of Noxa was p53-independent. On the other hand, PPD also induced prosurvival mechanisms including autophagy and expression of Bcl2 family apoptosis regulator Mcl-1. Inhibition of autophagy or knockdown of Mcl-1 significantly enhanced PPD-induced cell death. Interestingly, PPD inhibited expression of genes involved in fatty acid and cholesterol biosynthesis and induced synergistic cancer cell death with fatty acid synthase inhibitor cerulenin. As PPD-induced ER stress was not significantly affected by inhibition of new protein synthesis, we suggest PPD may induce ER stress directly through causing lipid disequilibrium.
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