Doxorubicin, vincristine, and actinomycin-D, but not teniposide, require long-lasting uninterrupted verapamil pressure to overcome drug resistance in multidrug-resistant cells.

G. Toffoli, L. Tumiotto, M. Gigante, T. Perin, G. Biscontin, M. Boiocchi

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The cytotoxic efficacy of doxorubicin (DOX), vincristine (VCR), actinomycin-D (ACT-D), and teniposide (VM-26) toward the LoVo and SW948 multidrug-resistant (MDR) cell sublines was significantly enhanced by the concomitant presence of verapamil (VER) during pharmacological treatment (1-h exposure) without, however, achieving a complete reversion of the MDR phenotype. Long-lasting VER in the culture medium, at the end of the combined drug+VER treatment, conferred to DOX, VCR, and ACT-D cytotoxic efficacy roughly similar to that exerted on the drug-sensitive parent cell lines. On the contrary, no enhancement of VM-26 cytotoxic efficacy was derived from continuous VER treatment. Enhancement of DOX, VCR, and ACT-D cytotoxic efficacy requires that VER be present in an uninterrupted manner in the culture medium since brief interruptions (15 to 60 min) in the VER pressure completely counteract any effect. These findings offer new insight into the modalities of pharmacological treatment that MDR cells require to obtain a complete reversion of cellular resistance to the various drug families included in the MDR spectrum.

Original languageEnglish
Pages (from-to)425-432
Number of pages8
JournalCancer Detection and Prevention
Volume17
Issue number3
Publication statusPublished - 1993

Fingerprint

Teniposide
Dactinomycin
Vincristine
Verapamil
Drug Resistance
Doxorubicin
Pressure
Culture Media
Pharmaceutical Preparations
Pharmacology
Phenotype
Cell Line

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

@article{71880d44e92f4bc7a6ed72edaa78ab1c,
title = "Doxorubicin, vincristine, and actinomycin-D, but not teniposide, require long-lasting uninterrupted verapamil pressure to overcome drug resistance in multidrug-resistant cells.",
abstract = "The cytotoxic efficacy of doxorubicin (DOX), vincristine (VCR), actinomycin-D (ACT-D), and teniposide (VM-26) toward the LoVo and SW948 multidrug-resistant (MDR) cell sublines was significantly enhanced by the concomitant presence of verapamil (VER) during pharmacological treatment (1-h exposure) without, however, achieving a complete reversion of the MDR phenotype. Long-lasting VER in the culture medium, at the end of the combined drug+VER treatment, conferred to DOX, VCR, and ACT-D cytotoxic efficacy roughly similar to that exerted on the drug-sensitive parent cell lines. On the contrary, no enhancement of VM-26 cytotoxic efficacy was derived from continuous VER treatment. Enhancement of DOX, VCR, and ACT-D cytotoxic efficacy requires that VER be present in an uninterrupted manner in the culture medium since brief interruptions (15 to 60 min) in the VER pressure completely counteract any effect. These findings offer new insight into the modalities of pharmacological treatment that MDR cells require to obtain a complete reversion of cellular resistance to the various drug families included in the MDR spectrum.",
author = "G. Toffoli and L. Tumiotto and M. Gigante and T. Perin and G. Biscontin and M. Boiocchi",
year = "1993",
language = "English",
volume = "17",
pages = "425--432",
journal = "Cancer Detection and Prevention",
issn = "0361-090X",
publisher = "Elsevier BV",
number = "3",

}

TY - JOUR

T1 - Doxorubicin, vincristine, and actinomycin-D, but not teniposide, require long-lasting uninterrupted verapamil pressure to overcome drug resistance in multidrug-resistant cells.

AU - Toffoli, G.

AU - Tumiotto, L.

AU - Gigante, M.

AU - Perin, T.

AU - Biscontin, G.

AU - Boiocchi, M.

PY - 1993

Y1 - 1993

N2 - The cytotoxic efficacy of doxorubicin (DOX), vincristine (VCR), actinomycin-D (ACT-D), and teniposide (VM-26) toward the LoVo and SW948 multidrug-resistant (MDR) cell sublines was significantly enhanced by the concomitant presence of verapamil (VER) during pharmacological treatment (1-h exposure) without, however, achieving a complete reversion of the MDR phenotype. Long-lasting VER in the culture medium, at the end of the combined drug+VER treatment, conferred to DOX, VCR, and ACT-D cytotoxic efficacy roughly similar to that exerted on the drug-sensitive parent cell lines. On the contrary, no enhancement of VM-26 cytotoxic efficacy was derived from continuous VER treatment. Enhancement of DOX, VCR, and ACT-D cytotoxic efficacy requires that VER be present in an uninterrupted manner in the culture medium since brief interruptions (15 to 60 min) in the VER pressure completely counteract any effect. These findings offer new insight into the modalities of pharmacological treatment that MDR cells require to obtain a complete reversion of cellular resistance to the various drug families included in the MDR spectrum.

AB - The cytotoxic efficacy of doxorubicin (DOX), vincristine (VCR), actinomycin-D (ACT-D), and teniposide (VM-26) toward the LoVo and SW948 multidrug-resistant (MDR) cell sublines was significantly enhanced by the concomitant presence of verapamil (VER) during pharmacological treatment (1-h exposure) without, however, achieving a complete reversion of the MDR phenotype. Long-lasting VER in the culture medium, at the end of the combined drug+VER treatment, conferred to DOX, VCR, and ACT-D cytotoxic efficacy roughly similar to that exerted on the drug-sensitive parent cell lines. On the contrary, no enhancement of VM-26 cytotoxic efficacy was derived from continuous VER treatment. Enhancement of DOX, VCR, and ACT-D cytotoxic efficacy requires that VER be present in an uninterrupted manner in the culture medium since brief interruptions (15 to 60 min) in the VER pressure completely counteract any effect. These findings offer new insight into the modalities of pharmacological treatment that MDR cells require to obtain a complete reversion of cellular resistance to the various drug families included in the MDR spectrum.

UR - http://www.scopus.com/inward/record.url?scp=0027352989&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027352989&partnerID=8YFLogxK

M3 - Article

C2 - 8402730

AN - SCOPUS:0027352989

VL - 17

SP - 425

EP - 432

JO - Cancer Detection and Prevention

JF - Cancer Detection and Prevention

SN - 0361-090X

IS - 3

ER -