Characterization of drug resistance to VM-26 in A2780 ovarian carcinoma cells

Chun Mao Lin, Tzong Yueh Chen, Leng Fang Wang, Cho Fat Hui, Jaulang Hwang

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Human ovarian carcinoma A2780 cells resistant to VM-26, a topoisomerase II-targeting drug, were cloned. Cross-resistance test showed that the resistant cells were 300 fold more tolerant toward VM-26 than were parental cells, whereas tolerance towards other drugs increased only 3 to 10 fold. VM-26 triggered apoptosis in a variety of cells including rodent cells, but not in resistant cells. This resistance might not be due to multidrug resistance (MDR). The topoisomerase II mRNA levels showed only a slight variation between VM-26-treated and -untreated resistant cells, and the difference in protein levels was about 2 fold. This implies that the level of topoisomerase IIβ expression may be unrelated to drug resistance. The DNA strand-passing activity of topoisomerase II affected by VM-26 was measured by K-SDS precipitation of the topoisomerase II-DNA complex, and topoisomerase II decatenation of kinetoplastic DNA (K-DNA). The results showed that the VM-26 influence on topoisomerase II cleavable activity was much less in resistant cells. Alteration of drug targeting sites in topoisomerase II might be a factor contributing to VM-26 drug resistance in these resistant cells.

Original languageEnglish
Pages (from-to)71-78
Number of pages8
JournalZoological Studies
Volume40
Issue number1
Publication statusPublished - Jan 2001

Fingerprint

DNA topoisomerase (ATP-hydrolysing)
drug resistance
carcinoma
cells
drugs
multiple drug resistance
cross resistance
DNA
rodents
apoptosis

Keywords

  • Drug resistance
  • Topoisomerase II
  • VM-26

ASJC Scopus subject areas

  • Animal Science and Zoology

Cite this

Lin, C. M., Chen, T. Y., Wang, L. F., Hui, C. F., & Hwang, J. (2001). Characterization of drug resistance to VM-26 in A2780 ovarian carcinoma cells. Zoological Studies, 40(1), 71-78.

Characterization of drug resistance to VM-26 in A2780 ovarian carcinoma cells. / Lin, Chun Mao; Chen, Tzong Yueh; Wang, Leng Fang; Hui, Cho Fat; Hwang, Jaulang.

In: Zoological Studies, Vol. 40, No. 1, 01.2001, p. 71-78.

Research output: Contribution to journalArticle

Lin, CM, Chen, TY, Wang, LF, Hui, CF & Hwang, J 2001, 'Characterization of drug resistance to VM-26 in A2780 ovarian carcinoma cells', Zoological Studies, vol. 40, no. 1, pp. 71-78.
Lin, Chun Mao ; Chen, Tzong Yueh ; Wang, Leng Fang ; Hui, Cho Fat ; Hwang, Jaulang. / Characterization of drug resistance to VM-26 in A2780 ovarian carcinoma cells. In: Zoological Studies. 2001 ; Vol. 40, No. 1. pp. 71-78.
@article{3c9dfec6497240638f2fbb48b4695cd6,
title = "Characterization of drug resistance to VM-26 in A2780 ovarian carcinoma cells",
abstract = "Human ovarian carcinoma A2780 cells resistant to VM-26, a topoisomerase II-targeting drug, were cloned. Cross-resistance test showed that the resistant cells were 300 fold more tolerant toward VM-26 than were parental cells, whereas tolerance towards other drugs increased only 3 to 10 fold. VM-26 triggered apoptosis in a variety of cells including rodent cells, but not in resistant cells. This resistance might not be due to multidrug resistance (MDR). The topoisomerase II mRNA levels showed only a slight variation between VM-26-treated and -untreated resistant cells, and the difference in protein levels was about 2 fold. This implies that the level of topoisomerase IIβ expression may be unrelated to drug resistance. The DNA strand-passing activity of topoisomerase II affected by VM-26 was measured by K-SDS precipitation of the topoisomerase II-DNA complex, and topoisomerase II decatenation of kinetoplastic DNA (K-DNA). The results showed that the VM-26 influence on topoisomerase II cleavable activity was much less in resistant cells. Alteration of drug targeting sites in topoisomerase II might be a factor contributing to VM-26 drug resistance in these resistant cells.",
keywords = "Drug resistance, Topoisomerase II, VM-26",
author = "Lin, {Chun Mao} and Chen, {Tzong Yueh} and Wang, {Leng Fang} and Hui, {Cho Fat} and Jaulang Hwang",
year = "2001",
month = "1",
language = "English",
volume = "40",
pages = "71--78",
journal = "Zoological Studies",
issn = "1021-5506",
publisher = "Biodiversity Research Center, Academia Sinica",
number = "1",

}

TY - JOUR

T1 - Characterization of drug resistance to VM-26 in A2780 ovarian carcinoma cells

AU - Lin, Chun Mao

AU - Chen, Tzong Yueh

AU - Wang, Leng Fang

AU - Hui, Cho Fat

AU - Hwang, Jaulang

PY - 2001/1

Y1 - 2001/1

N2 - Human ovarian carcinoma A2780 cells resistant to VM-26, a topoisomerase II-targeting drug, were cloned. Cross-resistance test showed that the resistant cells were 300 fold more tolerant toward VM-26 than were parental cells, whereas tolerance towards other drugs increased only 3 to 10 fold. VM-26 triggered apoptosis in a variety of cells including rodent cells, but not in resistant cells. This resistance might not be due to multidrug resistance (MDR). The topoisomerase II mRNA levels showed only a slight variation between VM-26-treated and -untreated resistant cells, and the difference in protein levels was about 2 fold. This implies that the level of topoisomerase IIβ expression may be unrelated to drug resistance. The DNA strand-passing activity of topoisomerase II affected by VM-26 was measured by K-SDS precipitation of the topoisomerase II-DNA complex, and topoisomerase II decatenation of kinetoplastic DNA (K-DNA). The results showed that the VM-26 influence on topoisomerase II cleavable activity was much less in resistant cells. Alteration of drug targeting sites in topoisomerase II might be a factor contributing to VM-26 drug resistance in these resistant cells.

AB - Human ovarian carcinoma A2780 cells resistant to VM-26, a topoisomerase II-targeting drug, were cloned. Cross-resistance test showed that the resistant cells were 300 fold more tolerant toward VM-26 than were parental cells, whereas tolerance towards other drugs increased only 3 to 10 fold. VM-26 triggered apoptosis in a variety of cells including rodent cells, but not in resistant cells. This resistance might not be due to multidrug resistance (MDR). The topoisomerase II mRNA levels showed only a slight variation between VM-26-treated and -untreated resistant cells, and the difference in protein levels was about 2 fold. This implies that the level of topoisomerase IIβ expression may be unrelated to drug resistance. The DNA strand-passing activity of topoisomerase II affected by VM-26 was measured by K-SDS precipitation of the topoisomerase II-DNA complex, and topoisomerase II decatenation of kinetoplastic DNA (K-DNA). The results showed that the VM-26 influence on topoisomerase II cleavable activity was much less in resistant cells. Alteration of drug targeting sites in topoisomerase II might be a factor contributing to VM-26 drug resistance in these resistant cells.

KW - Drug resistance

KW - Topoisomerase II

KW - VM-26

UR - http://www.scopus.com/inward/record.url?scp=0035218970&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035218970&partnerID=8YFLogxK

M3 - Article

VL - 40

SP - 71

EP - 78

JO - Zoological Studies

JF - Zoological Studies

SN - 1021-5506

IS - 1

ER -