ArticleJournal of ginseng research2025
Protopanaxatriol, a ginsenoside metabolite, induces apoptosis in colorectal cancer cells and arrests their cell cycle by targeting AKT.
Article in Journal of ginseng research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Ginsenosides Rh2 and Rg3 in first-line combination therapy: Prospects for rapid clinical translation in drug-resistant triple-negative breast cancer.Journal of ginseng research · 2026Review
- Emerging and underexplored ginsenosides in cancer therapy (2020-2025): Beyond cytotoxic mechanisms.Journal of ginseng research · 2026Review
- Ginsenosides fromJournal of ginseng research · 2026Review
- Protopanaxatriol enhances mucin expression in intestinal epithelial cells and mice.Journal of ginseng research · 2026Article
- SFTA2 reduced colorectal cancer ferroptosis promoting metastasis through regulating EMT transition by degradation of Nrf2.Food & nutrition research · 2026Article
- Pharmacokinetics and pharmacological activities of protopanaxatriol.Journal of ginseng research · 2025Review
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Authors and funding
8 authors.
Funding
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Abstract
Background: Colorectal cancer is the third most common cancer worldwide and the fourth leading cause of cancer death. Protopanaxatriol (PPT), one of the main active metabolic ginsenosides of ginseng, has been found to have neuroprotective and anti-inflammatory effects, but its role in regulating colon cancer development remained unclear. Purpose: We sought to confirm the inhibitory effect of PPT on colon cancer cells and elucidate its target and mechanism. Methods: MTT assay, colony formation, invasion, migration assays, cell apoptosis, and cell-cycle analysis were performed. Quantitative real-time PCR, Western blotting, bioinformatic analysis using the Kyoto Encyclopedia of Genes and Genomes and Gene Ontology, and cellular thermal shift assay experiments were also employed. Results: PPT can inhibit the cloning, migration, invasion, and proliferation of colon cancer cells. PPT can increase the number of apoptotic bodies, promote the expression of the apoptotic proteins caspase-9 and caspase-3, induce apoptosis, and inhibit cell proliferation. In addition, by regulating cyclin, PPT can increase the expression of p21 and p27 proteins and inhibit the expression of the cyclin D1 protein, thereby inhibiting the G1/S transformation in the cell cycle. We further demonstrated that PPT can target AKT, reduce its protein expression, and reduce tumor progression and the expression of inflammatory factors caused by AKT high expression (TNF-α, IL-1β, and IL-6), thereby playing a role in inhibiting colon cancer progression. Conclusion: We are the first to demonstrate that the ginsenoside PPT can inhibit the activity of colon cancer cells by directly binding AKT.
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