当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > Markedly decreased binding of vincristine to tubulin in vinca alkaloid-resistant Chinese hamster cells is associated with selective overexpression of alpha and beta tubulin isoforms.

Markedly decreased binding of vincristine to tubulin in vinca alkaloid-resistant Chinese hamster cells is associated with selective overexpression of alpha and beta tubulin isoforms.

Abstract：

:Vinca alkaloids are among a number of cytotoxic agents which target tumor cell microtubules. Studies described herein document the basis for one form of acquired resistance to these plant alkaloids involving an alteration of tubulin in a variant (DC-3F/VCRd-5L) of DC-3F Chinese hamster cells. Our results revealed a markedly decreased binding of [(3)H]vincristine (VCR) to tubulin extracted from this variant compared to tubulin extracted from wild-type DC-3F cells. This was quantitated as a 10- to 15-fold decrease in on-rate in the presence of GTP for the [(3)H]VCR associating with tubulin in cell-free cytosol and a 10-fold increase in off-rate for GTP-dependent dissociation of the [(3)H]VCR-tubulin complex. Quantitative RT-PCR and nucleotide sequencing of poly(A)(+) RNA also carried out with variant and wild-type DC-3F cells documented a different pattern of relative expression, but no base pair differences in the open reading frame of the three alpha and beta tubulin isoforms detected in each cell type. This was accounted for by selective overexpression of one alpha tubulin (alphaII) and two beta tubulin (betaI and betaIV) isoforms in the variant cells. These results would appear to provide an underlying basis for the large decrease in [(3)H]VCR binding by tubulin in these variant Chinese hamster cells and a major component of their acquired resistance to this vinca alkaloid.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Sirotnak FM,Danenberg KD,Chen J,Fritz F,Danenberg PV

doi

10.1006/bbrc.2000.2246

subject

Has Abstract

pub_date

2000-03-05 00:00:00

pages

21-4

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(00)92246-0

journal_volume

269

pub_type

杂志文章

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