ArticleInternational journal of molecular sciences2010
Compound K, a metabolite of ginseng saponin, induces mitochondria-dependent and caspase-dependent apoptosis via the generation of reactive oxygen species in human colon cancer cells.
Article in International journal of molecular sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 54 citations in OpenAlex.
- Compound K-enriched Korean red ginseng prevents lung cancer progression by targeting cancer cells and fibroblasts.Journal of ginseng research · 2025Article
- Article
- Potential Anti-tumor Effects and Apoptosis-inducing Mechanisms of Saponins: A Review.Current topics in medicinal chemistry · 2025Review
- Anticancer properties and pharmaceutical applications of ginsenoside compound K: A review.Chemical biology & drug design · 2022Review
- A narrative review of the pharmacology of ginsenoside compound K.Annals of translational medicine · 2022Review
- The promising therapeutic potentials of ginsenosides mediated through p38 MAPK signaling inhibition.Heliyon · 2021Review
- Ginsenosides emerging as both bifunctional drugs and nanocarriers for enhanced antitumor therapies.Journal of nanobiotechnology · 2021Review
- Saponins in Cancer Treatment: Current Progress and Future Prospects.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Review
- Review of ginsenosides targeting mitochondrial function to treat multiple disorders: Current status and perspectives.Journal of ginseng research · 2021Review
- Ginsenoside Compound K: Insights into Recent Studies on Pharmacokinetics and Health-Promoting Activities.Biomolecules · 2020Review
- Microbial Metabolites Determine Host Health and the Status of Some Diseases.International journal of molecular sciences · 2019Review
- Ginsenoside Compound K Induces Ros-Mediated Apoptosis and Autophagic Inhibition in Human Neuroblastoma Cells In Vitro and In Vivo.International journal of molecular sciences · 2019Article
- Ginsenoside compound K inhibits nuclear factor-kappa B by targeting Annexin A2.Journal of ginseng research · 2019Article
- Compound K induced apoptosis via endoplasmic reticulum CaJournal of ginseng research · 2018Article
- Review
- Article
- Enhanced antidiabetic efficacy and safety of compound K⁄β-cyclodextrin inclusion complex in zebrafish.Journal of ginseng research · 2017Article
- Ginsenoside compound K sensitizes human colon cancer cells to TRAIL-induced apoptosis via autophagy-dependent and -independent DR5 upregulation.Cell death & disease · 2016Article
- Anticancer Activities of Protopanaxadiol- and Protopanaxatriol-Type Ginsenosides and Their Metabolites.Evidence-based complementary and alternative medicine : eCAM · 2016Review
- Ginsenoside fractions regulate the action of monocytes and their differentiation into dendritic cells.Journal of ginseng research · 2015Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of this study was to elucidate the cytotoxic mechanism of Compound K, with respect to the involvement of reactive oxygen species (ROS) and the mitochondrial involved apoptosis, in HT-29 human colon cancer cells. Compound K exhibited a concentration of 50% growth inhibition (IC(50)) at 20 μg/mL and cytotoxicity in a time dependent manner. Compound K produced intracellular ROS in a time dependent fashion; however, N-acetylcysteine (NAC) pretreatment resulted in the inhibition of this effect and the recovery of cell viability. Compound K induced a mitochondria-dependent apoptotic pathway via the modulation of Bax and Bcl-2 expressions, resulting in the disruption of the mitochondrial membrane potential (Δψ(m)). Loss of the Δψ(m) was followed by cytochrome c release from the mitochondria, resulting in the activation of caspase-9, -3, and concomitant poly ADP-ribosyl polymerase (PARP) cleavage, which are the indicators of caspase-dependent apoptosis. The apoptotic effect of Compound K, exerted via the activation of c-Jun NH(2)-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), was abrogated by specific MAPK inhibitors. This study demonstrated that Compound K-mediated generation of ROS led to apoptosis through the modulation of a mitochondria-dependent apoptotic pathway and MAPK pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.