Evidence map›Paper›PMID 11850844›Full record

ArticleOncogene2002

Inhibition of tumour cell growth by hyperforin, a novel anticancer drug from St. John's wort that acts by induction of apoptosis.

Christoph M Schempp, Vladimir Kirkin, Birgit Simon-Haarhaus, Astrid Kersten, Judit Kiss, Christian C Termeer, Bernhard Gilb, Thomas Kaufmann, Christoph Borner, Jonathan P Sleeman and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
18.7field-weighted citation impact, top 1% 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

53 citing papers in PubMed, 262 citations in OpenAlex.

  1. Review
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  13. Cytotoxicity andHeliyon · 2022
    Article
  14. Article
  15. Cytotoxic activities ofCytotechnology · 2021
    Article
  16. Review
  17. Anti-Tumor Activity ofAntioxidants (Basel, Switzerland) · 2020
    Review
  18. Antiproliferative Effects of St. John's Wort, Its Derivatives, and OtherInternational journal of molecular sciences · 2020
    Review
  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

11 authors at 2 institutions in 1 country.

Christoph M SchemppDepartment of Dermatology, University of Freiburg, Hauptstrasse 7, D-79104 Freiburg, Germany. schempp@haut.ukl.uni-freiburg.de
Vladimir Kirkin
Birgit Simon-Haarhaus
Astrid Kersten
Judit Kiss
Christian C Termeer
Bernhard Gilb
Thomas Kaufmann
Christoph Borner
Jonathan P Sleeman
Jan C Simon
University of Freiburg · DEFZI Research Center for Information Technology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperforin is a plant derived antibiotic from St. John's wort. Here we describe a novel activity of hyperforin, namely its ability to inhibit the growth of tumour cells by induction of apoptosis. Hyperforin inhibited the growth of various human and rat tumour cell lines in vivo, with IC(50) values between 3-15 microM. Treatment of tumour cells with hyperforin resulted in a dose-dependent generation of apoptotic oligonucleosomes, typical DNA-laddering and apoptosis-specific morphological changes. In MT-450 mammary carcinoma cells hyperforin increased the activity of caspase-9 and caspase-3, and hyperforin-mediated apoptosis was blocked by the broad-range caspase inhibitor zVAD.fmk. When added to MT-450 cells, hyperforin, but not paclitaxel, induced a rapid loss of the mitochondrial transmembrane potential Deltapsi(m), and subsequent morphological changes such as homogenization and vacuolization of mitochondria. Monitoring of Deltapsi(m) revealed that the hyperforin-mediated mitochondrial permeability transition can not be prevented by zVAD.fmk. This indicates that mitochondrial permeabilization is a cause rather than a consequence of caspase activation. Moreover, hyperforin was capable of releasing cytochrome c from isolated mitochondria. These findings suggest that hyperforin activates a mitochondria-mediated apoptosis pathway. In vivo, hyperforin inhibited the growth of autologous MT-450 breast carcinoma in immunocompetent Wistar rats to a similar extent as the cytotoxic drug paclitaxel, without any signs of acute toxicity. Owing to the combination of significant antitumour activity, low toxicity in vivo and natural abundance of the compound, hyperforin holds the promise of being an interesting novel antineoplastic agent that deserves further laboratory and in vivo exploration.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBridged Bicyclo CompoundsCaspasesCell DivisionCytochrome c GroupDose-Response Relationship, DrugEnzyme ActivationFemaleHumansHypericumIntracellular MembranesMicroscopy, ElectronMitochondriaNeoplasmsAntineoplastic AgentsBridged Bicyclo CompoundsCaspasesCytochrome c GrouphyperforinPhloroglucinolStaurosporineTerpenes

Identifiers

PMID11850844
OpenAlexW1969345055

What OpenQuestion holds

Textmetadata
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.