ArticleArchives of pharmacal research2022
Ginsenoside Rh1 inhibits tumor growth in MDA-MB-231 breast cancer cells via mitochondrial ROS and ER stress-mediated signaling pathway.
Article in Archives of pharmacal research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Emerging and underexplored ginsenosides in cancer therapy (2020-2025): Beyond cytotoxic mechanisms.Journal of ginseng research · 2026Review
- 20(S/R)-Ginsenoside Rh1 Alleviates AOM/DSS-Induced Colorectal Cancer: Gut-Microbiota Modulation and Tryptophan-Metabolism-Mediated AhR/PXR Activation and IDO1.International journal of molecular sciences · 2026Article
- Research progress of ginseng active ingredients combined with chemotherapy in cancer therapy.Journal of ginseng research · 2026Review
- Targeting Autophagy in Ovarian Cancer: The Emerging Role of Ginsenosides.Cancer medicine · 2026Review
- Bioactive Constituents of Ginseng in Cancer Therapy: Molecular Mechanisms, Translational Potential, and Advanced Delivery Strategies.International journal of biological sciences · 2026Review
- Endoplasmic reticulum stress-mediated programmed cell death in the tumor microenvironment.Cell death discovery · 2025Review
- Ginsenoside Rh1 inhibits tumor growth in mice with colorectal cancer and depressive symptoms via modulation of the gut microbiota and tumor microenvironment.Molecular medicine reports · 2025Article
- Ginsenoside Rh2 as a novel PIN1 inhibitor disrupting the cancer stem cell-like phenotype in non-small cell lung cancer.Journal of translational medicine · 2025Article
- Ginseng-Based Nanotherapeutics in Cancer Treatment: State-of-the-Art Progress, Tackling Gaps, and Translational Achievements.Current issues in molecular biology · 2025Review
- Ginsenoside Rg3 activates the immune function of CD8+ T cells via circFOXP1-miR-4477a-PD-L1 axis to induce ferroptosis in gallbladder cancer.Archives of pharmacal research · 2024Article
- Ferroptosis as a promising targeted therapy for triple negative breast cancer.Breast cancer research and treatment · 2024Review
- Human milk oligosaccharides 3'-sialyllactose and 6'-sialyllactose attenuate LPS-induced lung injury by inhibiting STAT1 and NF-κB signaling pathways.Archives of pharmacal research · 2023Article
- Ginsenosides: changing the basic hallmarks of cancer cells to achieve the purpose of treating breast cancer.Chinese medicine · 2023Review
- Experimental model and novel therapeutic targets for non-alcoholic fatty liver disease development.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Review
- Anticancer therapeutic effect of ginsenosides through mediating reactive oxygen species.Frontiers in pharmacology · 2023Review
- 6'-Sialylactose abolished lipopolysaccharide-induced inflammation and hyper-permeability in endothelial cells.Archives of pharmacal research · 2022Article
- Anti-cancer effect and potential microRNAs targets of ginsenosides against breast cancer.Frontiers in pharmacology · 2022Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Ginsenoside-Rh1 (Rh1) is a ginseng-derived compound that has been reported to exert anticancer effects by regulating cell cycle arrest and apoptosis according to reactive oxygen species (ROS) production. However, the effects of Rh1 on mitochondrial dysfunction are involved in triple negative breast cancer (TNBC) cell apoptosis, and the related molecular mechanisms remain unknown. Rh1 treatment induced cell toxicity less than 50% at 50 μM. In addition, Rh1 induced apoptosis in TNBC cells through cleaved caspase-3 activation and G1/S arrest. The Rh1-treated TNBC cells showed a significant increase in mitochondrial ROS (mtROS), which in turn increased protein expression of mitochondrial molecules, such as Bak and cytochrome C, and caused the loss of mitochondrial membrane potential. Pretreatment with mitochondria-targeted antioxidant Mito-TEMPO alters the Rh1-reduced rate of mito- and glycol-ATP. Furthermore, Rh1 induces ER stress-mediated calcium accumulation via PERK/eIF2α/ATF4/CHOP pathway. Inhibition of ATF4 by siRNA transfection significantly inhibited Rh1-mediated apoptosis and calcium production. Interestingly, Mito-TEMPO treatment significantly reduced apoptosis and ER stress induced by Rh1. Finally, Rh1 at 5 mg/kg suppressed tumor growth through increased levels of ROS production, cleaved caspase-3, and ATF4 more than 5-fluorouracil treated group. Overall, our results suggest that Rh1 has potential for use in TNBC treatment.
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