REVERSAL OF DOXORUBICIN-RESISTANCE IN SARCOMA-180 TUMOR-CELLS BY INHIBITION OF DIFFERENT RESISTANCE MECHANISMS

Publication type:
Journal article
Metadata:
Autoren
  • T EFFERTH
  • M VOLM
Autoren-URL
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:A1993LT78800008&DestLinkType=FullRecord&DestApp=WOS_CPL
DOI
10.1016/0304-3835(93)90231-W
Externe Identifier
  • Clarivate Analytics Document Solution ID: LT788
  • PubMed Identifier: 8102593
ISSN
0304-3835
Ausgabe der Veröffentlichung
3
Zeitschrift
CANCER LETTERS
Schlüsselwörter
  • DOXORUBICIN
  • MULTIDRUG-RESISTANCE
  • REVERSAL OF RESISTANCE
Paginierung
197 - 202
Datum der Veröffentlichung
1993
Status
Published
Titel
REVERSAL OF DOXORUBICIN-RESISTANCE IN SARCOMA-180 TUMOR-CELLS BY INHIBITION OF DIFFERENT RESISTANCE MECHANISMS
Sub types
  • Article
Ausgabe der Zeitschrift
70

Data source: Web of Science (Lite)

Other metadata sources:
Autoren
  • T Efferth
  • M Volm
DOI
10.1016/0304-3835(93)90231-w
ISSN
0304-3835
Ausgabe der Veröffentlichung
3
Zeitschrift
Cancer Letters
Sprache
en
Paginierung
197 - 202
Datum der Veröffentlichung
1993
Status
Published
Herausgeber
Elsevier BV
Herausgeber URL
http://dx.doi.org/10.1016/0304-3835(93)90231-w
Datum der Datenerfassung
2021
Titel
Reversal of doxorubicin-resistance in sarcoma 180 tumor cells by inhibition of different resistance mechanisms
Ausgabe der Zeitschrift
70

Data source: Crossref

Abstract
Resistance of tumor cells to doxorubicin is a multifactorial phenomenon. In the present investigation, the ability of resistance modifiers against different resistance mechanisms was analysed. Substances which block P-glycoprotein (P-170) function circumvented resistance of doxorubicin-resistant sarcoma 180 (S180) cells completely (verapamil, thioridazine) or partially (hycanthone), whereas inhibitors of glutathione S-transferase (ethacrynic acid, N-ethylmaleimide, buthionine sulfoximine), and protein kinase C (staurosporine, acridine orange) caused only a partial reversion of resistance. In contrast, an inhibitor of alkaline phosphatase (levamisole) did not overcome doxorubicin-resistance. These results indicate that P-glycoprotein blockers might be more effective to modulate doxorubicin-resistance of S180 cells as compared to other modifiers. Further investigations using other MDR cell lines are required to clarify the generality of these findings.
Addresses
  • German Cancer Research Center, Heidelberg.
Autoren
DOI
10.1016/0304-3835(93)90231-w
eISSN
1872-7980
Externe Identifier
  • PubMed Identifier: 8102593
Open access
false
ISSN
0304-3835
Ausgabe der Veröffentlichung
3
Zeitschrift
Cancer letters
Schlüsselwörter
  • Tumor Cells, Cultured
  • Animals
  • Sarcoma 180
  • Doxorubicin
  • Alkaline Phosphatase
  • DNA Topoisomerases, Type II
  • Catalase
  • Glutathione Transferase
  • Protein Kinase C
  • Carrier Proteins
  • Membrane Glycoproteins
  • Radioimmunoassay
  • Immunohistochemistry
  • Cell Division
  • Dose-Response Relationship, Drug
  • Drug Resistance
  • Topoisomerase II Inhibitors
  • ATP Binding Cassette Transporter, Subfamily B, Member 1
Sprache
eng
Medium
Print
Paginierung
197 - 202
Datum der Veröffentlichung
1993
Status
Published
Datum der Datenerfassung
1993
Titel
Reversal of doxorubicin-resistance in sarcoma 180 tumor cells by inhibition of different resistance mechanisms.
Sub types
  • Journal Article
Ausgabe der Zeitschrift
70

Data source: Europe PubMed Central

Abstract
Resistance of tumor cells to doxorubicin is a multifactorial phenomenon. In the present investigation, the ability of resistance modifiers against different resistance mechanisms was analysed. Substances which block P-glycoprotein (P-170) function circumvented resistance of doxorubicin-resistant sarcoma 180 (S180) cells completely (verapamil, thioridazine) or partially (hycanthone), whereas inhibitors of glutathione S-transferase (ethacrynic acid, N-ethylmaleimide, buthionine sulfoximine), and protein kinase C (staurosporine, acridine orange) caused only a partial reversion of resistance. In contrast, an inhibitor of alkaline phosphatase (levamisole) did not overcome doxorubicin-resistance. These results indicate that P-glycoprotein blockers might be more effective to modulate doxorubicin-resistance of S180 cells as compared to other modifiers. Further investigations using other MDR cell lines are required to clarify the generality of these findings.
Autoren
  • T Efferth
  • M Volm
Autoren-URL
https://www.ncbi.nlm.nih.gov/pubmed/8102593
DOI
10.1016/0304-3835(93)90231-w
ISSN
0304-3835
Ausgabe der Veröffentlichung
3
Zeitschrift
Cancer Lett
Schlüsselwörter
  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • Alkaline Phosphatase
  • Animals
  • Carrier Proteins
  • Catalase
  • Cell Division
  • DNA Topoisomerases, Type II
  • Dose-Response Relationship, Drug
  • Doxorubicin
  • Drug Resistance
  • Glutathione Transferase
  • Immunohistochemistry
  • Membrane Glycoproteins
  • Protein Kinase C
  • Radioimmunoassay
  • Sarcoma 180
  • Topoisomerase II Inhibitors
  • Tumor Cells, Cultured
Sprache
eng
Country
Ireland
Paginierung
197 - 202
PII
0304-3835(93)90231-W
Datum der Veröffentlichung
1993
Status
Published
Datum, an dem der Datensatz öffentlich gemacht wurde
1993
Titel
Reversal of doxorubicin-resistance in sarcoma 180 tumor cells by inhibition of different resistance mechanisms.
Sub types
  • Journal Article
Ausgabe der Zeitschrift
70

Data source: PubMed

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