Evidence map›Paper›PMID 20017956›Full record

ArticleBMC cancer2009

Compound K, a metabolite of ginseng saponin, induces apoptosis via caspase-8-dependent pathway in HL-60 human leukemia cells.

Sung-Hee Cho, Kyung-Sook Chung, Jung-Hye Choi, Dong-Hyun Kim, Kyung-Tae Lee

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Effects of Protease-Hydrolyzed andFoods (Basel, Switzerland) · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Recent trends in ginseng research.Journal of natural medicines · 2024
    Review
  8. Article
  9. Anti-leukemia effects of ginsenoside monomer: A narrative review of pharmacodynamics study.Current therapeutic research, clinical and experimental · 2024
    Review
  10. Review
  11. Article
  12. Review
  13. Saponins in Cancer Treatment: Current Progress and Future Prospects.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Sung-Hee ChoDepartment of Pharmaceutical Biochemistry, College of Pharmacy, Kyung-Hee University, Seoul 130-701, South Korea.
Kyung-Sook Chung
Jung-Hye Choi
Dong-Hyun Kim
Kyung-Tae Lee
Kyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCompound K [20-O-beta-(D-glucopyranosyl)-20(S)-protopanaxadiol], a metabolite of the protopanaxadiol-type saponins of Panax ginseng C.A. Meyer, has been reported to possess anti-tumor properties to inhibit angiogenesis and to induce tumor apoptosis. In the present study, we investigated the effect of Compound K on apoptosis and explored the underlying mechanisms involved in HL-60 human leukemia cells.

methodsWe examined the effect of Compound K on the viabilities of various cancer cell lines using MTT assays. DAPI assay, Annexin V and PI double staining, Western blot assay and immunoprecipitation were used to determine the effect of Compound K on the induction of apoptosis.

resultsCompound K was found to inhibit the viability of HL-60 cells in a dose- and time-dependent manner with an IC50 of 14 muM. Moreover, this cell death had typical features of apoptosis, that is, DNA fragmentation, DNA ladder formation, and the externalization of Annexin V targeted phosphatidylserine residues in HL-60 cells. In addition, compound-K induced a series of intracellular events associated with both the mitochondrial- and death receptor-dependent apoptotic pathways, namely, (1) the activation of caspases-3, -8, and -9; (2) the loss of mitochondrial membrane potential; (3) the release of cytochrome c and Smac/DIABLO to the cytosol; (4) the translocation of Bid and Bax to mitochondria; and (5) the downregulations of Bcl-2 and Bcl-xL. Furthermore, a caspase-8 inhibitor completely abolished caspase-3 activation, Bid cleavage, and subsequent DNA fragmentation by Compound K. Interestingly, the activation of caspase-3 and -8 and DNA fragmentation were significantly prevented in the presence of cycloheximide, suggesting that Compound K-induced apoptosis is dependent on de novo protein synthesis.

conclusionsThe results indicate that caspase-8 plays a key role in Compound K-stimulated apoptosis via the activation of caspase-3 directly or indirectly through Bid cleavage, cytochrome c release, and caspase-9 activation.

Indexed as

ApoptosisApoptosis Regulatory ProteinsCaspase 8Cytochromes cDrug Evaluation, PreclinicalGinsenosidesHeLa CellsHL-60 CellsHumansIntracellular Signaling Peptides and ProteinsLeukemiaMembrane PotentialsMitochondrial ProteinsModels, BiologicalPanaxSaponinsApoptosis Regulatory ProteinsCASP8 protein, humanCaspase 8Cytochromes cDIABLO protein, humanginsenoside compound KGinsenosidesIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsSaponins

Identifiers

PMID20017956
PMCPMC2806409
OpenAlexW2043752864

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.