ArticleMolecular medicine reports2018
Ginsenoside Rh2 inhibits human A172 glioma cell proliferation and induces cell cycle arrest status via modulating Akt signaling pathway.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 29 citations in OpenAlex.
- Bioactive Constituents of Ginseng in Cancer Therapy: Molecular Mechanisms, Translational Potential, and Advanced Delivery Strategies.International journal of biological sciences · 2026Review
- Immunometabolism and oxidative stress: roles and therapeutic strategies in cancer and aging.npj aging · 2025Review
- Gasdermin D Plays an Oncogenic Role in Glioma and Correlates to an Immunosuppressive Microenvironment.Biomolecules · 2023Article
- The effects of Ginsenosides on PI3K/AKT signaling pathway.Molecular biology reports · 2022Review
- Metabonomic profiling of clubroot-susceptible and clubroot-resistant radish and the assessment of disease-resistant metabolites.Frontiers in plant science · 2022Article
- 20(Journal of ginseng research · 2021Article
- Gallic Acid Suppressed Tumorigenesis by an LncRNA MALAT1-Wnt/β-Catenin Axis in Hepatocellular Carcinoma.Frontiers in pharmacology · 2021Article
- Inhibitory Effects of Ginsenoside Ro on the Growth of B16F10 Melanoma via Its Metabolites.Molecules (Basel, Switzerland) · 2019Article
- Natural Product Triterpenoids and Their Semi-Synthetic Derivatives with Potential Anticancer Activity.Planta medica · 2019Review
- Reversal effect of ginsenoside Rh2 on oxaliplatin-resistant colon cancer cells and its mechanism.Experimental and therapeutic medicine · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ginsenoside Rh2 (G‑Rh2), the main bioactive component in American ginseng, is known to exert a wide variety of biological activities. Accumulating evidence suggests that G‑Rh2 inhibits cell proliferation and induces apoptosis of tumor cells. However, the possible mechanism through which G‑Rh2 exerts its action on malignant glioma cells have not been completely elucidated. The findings of the present study demonstrated that G‑Rh2 decreased the viability of glioma cells in a dose‑ and time‑dependent manner, and induced cell cycle arrest. G‑Rh2‑induced cell cycle arrest was accompanied by the downregulation of cyclin‑dependent kinase 4 and Cyclin E. In addition, G‑Rh2 markedly reduced the expression of total‑ RAC‑α serine/threonine‑protein kinase (Akt) and the levels of phosphorylated‑Akt. These findings provide mechanistic details of how G‑Rh2 acts on glioma cells and suggest that G‑Rh2 may function as a potential anti‑cancer drug for glioma treatment.
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