ArticleMolecules (Basel, Switzerland)2022
(20S) Ginsenoside Rh2-Activated, Distinct Apoptosis Pathways in Highly and Poorly Differentiated Human Esophageal Cancer Cells.
Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Tumor-targeted liposomal RNAi therapy suppresses breast cancer and modulates tumor microenvironment.Journal of nanobiotechnology · 2026Article
- Bioactive Constituents of Ginseng in Cancer Therapy: Molecular Mechanisms, Translational Potential, and Advanced Delivery Strategies.International journal of biological sciences · 2026Review
- Ginsenoside Rh2 targets SIRT1-mediated deacetylation to modulate ERα/AR balance and overcome endocrine therapy resistance in prostate cancer using 3D organoid models.Cell biology and toxicology · 2025Article
- Natural anti-cancer products: insights from herbal medicine.Chinese medicine · 2025Review
- Network pharmacology, prognostic analysis and experimental validation elucidate the therapeutic mechanism of Dingxiang Guanshitong in esophageal cancer.Scientific reports · 2025Article
- Ginseng-Based Nanotherapeutics in Cancer Treatment: State-of-the-Art Progress, Tackling Gaps, and Translational Achievements.Current issues in molecular biology · 2025Review
- Computer-driven formulation development of Ginsenoside Rh2 ternary solid dispersion.Drug delivery and translational research · 2025Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Ginsenoside Rh2 (G-Rh2), a rare ginsenoside isolated from red ginseng, has considerable anti-cancer activity and induces apoptosis in a variety of cancer cells, but its activity in esophageal cancer cells is unclear. In this study, we examined the cytotoxic activity of (20S) G-Rh2 in highly differentiated esophageal squamous ECA109 cells and poorly differentiated esophageal squamous TE-13 cells. (20S) G-Rh2 exerted intense cytotoxicity in ECA109 and TE-13 cells with an IC50 of 2.9 and 3.7 μg/mL, respectively. After treatment with G-Rh2, Bcl-2, and Bcl-xL, the two main anti-apoptosis Bcl-2 family proteins upregulated, and Bax and Bak, the two key pro-apoptosis proteins translocated to mitochondria in both cell lines. At the same time, cytochrome
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