Molecular modes of action of cantharidin in tumor cells
- Publikationstyp:
- Zeitschriftenaufsatz
- Metadaten:
-
- Autoren
- T Efferth
- R Rauh
- S Kahl
- M Tomicic
- H Böchzelt
- ME Tome
- MM Briehl
- R Bauer
- B Kaina
- Autoren-URL
- https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000227371400010&DestLinkType=FullRecord&DestApp=WOS_CPL
- DOI
- 10.1016/j.bcp.2004.12.003
- Externe Identifier
- Clarivate Analytics Document Solution ID: 902QK
- PubMed Identifier: 15710358
- ISSN
- 0006-2952
- Ausgabe der Veröffentlichung
- 5
- Zeitschrift
- BIOCHEMICAL PHARMACOLOGY
- Schlüsselwörter
- apoptosis
- cancer chemotherapy
- DNA repair
- natural compounds
- oxidative stress
- Paginierung
- 811 - 818
- Datum der Veröffentlichung
- 2005
- Status
- Published
- Titel
- Molecular modes of action of cantharidin in tumor cells
- Sub types
- Article
- Ausgabe der Zeitschrift
- 69
Datenquelle: Web of Science (Lite)
- Andere Metadatenquellen:
-
- Autoren
- Thomas Efferth
- Rolf Rauh
- Stefan Kahl
- Maja Tomicic
- Herbert Böchzelt
- Margaret E Tome
- Margaret M Briehl
- Rudolf Bauer
- Bernd Kaina
- DOI
- 10.1016/j.bcp.2004.12.003
- ISSN
- 0006-2952
- Ausgabe der Veröffentlichung
- 5
- Zeitschrift
- Biochemical Pharmacology
- Sprache
- en
- Paginierung
- 811 - 818
- Datum der Veröffentlichung
- 2005
- Status
- Published
- Herausgeber
- Elsevier BV
- Herausgeber URL
- http://dx.doi.org/10.1016/j.bcp.2004.12.003
- Datum der Datenerfassung
- 2019
- Titel
- Molecular modes of action of cantharidin in tumor cells
- Ausgabe der Zeitschrift
- 69
Datenquelle: Crossref
- Abstract
- Cancer chemotherapy is often limited by patient's toxicity and tumor drug resistance indicating that new drug development and modification of existing drugs is critical for improving the therapeutic response. Traditional Chinese medicine is a rich source of potential anticancer agents. In particular, cantharidin (CAN), the active principle ingredient from the blister beetle, Mylabris, has anti-tumor activity, but the cytotoxic mechanism is unknown. In leukemia cells, cantharidin induces apoptosis by a p53-dependent mechanism. Cantharidin causes both DNA single- and double-strand breaks. Colony-forming assays with knockout and transfectant cells lines showed that DNA polymerase beta, but not ERCC1, conferred increased cell survival after cantharidin treatment, indicating that base excision repair (BER), rather than nucleotide excision repair (NER), is important for CAN-induced DNA lesions. Oxidative stress-resistant thymic lymphoma-derived WEHI7.2 variants are also more resistant to cantharidin. These data suggest that cantharidin treatment causes oxidative stress that provokes DNA damage and p53-dependent apoptosis.
- Addresses
- German Cancer Research Center, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. thomas.efferth@web.de
- Autoren
- Thomas Efferth
- Thomas Efferth
- Rolf Rauh
- Stefan Kahl
- Maja Tomicic
- Herbert Böchzelt
- Margaret E Tome
- Margaret M Briehl
- Rudolf Bauer
- Bernd Kaina
- DOI
- 10.1016/j.bcp.2004.12.003
- eISSN
- 1873-2968
- Externe Identifier
- PubMed Identifier: 15710358
- Open access
- false
- ISSN
- 0006-2952
- Ausgabe der Veröffentlichung
- 5
- Zeitschrift
- Biochemical pharmacology
- Schlüsselwörter
- Cell Line, Tumor
- Humans
- DNA Damage
- Cantharidin
- Endonucleases
- DNA-Binding Proteins
- Antineoplastic Agents
- Apoptosis
- DNA Repair
- Oxidative Stress
- Sprache
- eng
- Medium
- Print-Electronic
- Online publication date
- 2005
- Paginierung
- 811 - 818
- Datum der Veröffentlichung
- 2005
- Status
- Published
- Datum der Datenerfassung
- 2005
- Titel
- Molecular modes of action of cantharidin in tumor cells.
- Sub types
- Journal Article
- Ausgabe der Zeitschrift
- 69
Datenquelle: Europe PubMed Central
- Abstract
- Cancer chemotherapy is often limited by patient's toxicity and tumor drug resistance indicating that new drug development and modification of existing drugs is critical for improving the therapeutic response. Traditional Chinese medicine is a rich source of potential anticancer agents. In particular, cantharidin (CAN), the active principle ingredient from the blister beetle, Mylabris, has anti-tumor activity, but the cytotoxic mechanism is unknown. In leukemia cells, cantharidin induces apoptosis by a p53-dependent mechanism. Cantharidin causes both DNA single- and double-strand breaks. Colony-forming assays with knockout and transfectant cells lines showed that DNA polymerase beta, but not ERCC1, conferred increased cell survival after cantharidin treatment, indicating that base excision repair (BER), rather than nucleotide excision repair (NER), is important for CAN-induced DNA lesions. Oxidative stress-resistant thymic lymphoma-derived WEHI7.2 variants are also more resistant to cantharidin. These data suggest that cantharidin treatment causes oxidative stress that provokes DNA damage and p53-dependent apoptosis.
- Date of acceptance
- 2004
- Autoren
- Thomas Efferth
- Rolf Rauh
- Stefan Kahl
- Maja Tomicic
- Herbert Böchzelt
- Margaret E Tome
- Margaret M Briehl
- Rudolf Bauer
- Bernd Kaina
- Autoren-URL
- https://www.ncbi.nlm.nih.gov/pubmed/15710358
- DOI
- 10.1016/j.bcp.2004.12.003
- ISSN
- 0006-2952
- Ausgabe der Veröffentlichung
- 5
- Zeitschrift
- Biochem Pharmacol
- Schlüsselwörter
- Antineoplastic Agents
- Apoptosis
- Cantharidin
- Cell Line, Tumor
- DNA Damage
- DNA Repair
- DNA-Binding Proteins
- Endonucleases
- Humans
- Oxidative Stress
- Sprache
- eng
- Country
- England
- Paginierung
- 811 - 818
- PII
- S0006-2952(04)00819-6
- Datum der Veröffentlichung
- 2005
- Status
- Published
- Datum, an dem der Datensatz öffentlich gemacht wurde
- 2005
- Titel
- Molecular modes of action of cantharidin in tumor cells.
- Sub types
- Journal Article
- Ausgabe der Zeitschrift
- 69
Datenquelle: PubMed
- Beziehungen:
- Eigentum von