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Antiproliferative activity of ecteinascidin 743 is dependent upon transcription-coupled nucleotide-excision repair.

Abstract：

:While investigating the novel anticancer drug ecteinascidin 743 (Et743), a natural marine product isolated from the Caribbean sea squirt, we discovered a new cell-killing mechanism mediated by DNA nucleotide excision repair (NER). A cancer cell line selected for resistance to Et743 had chromosome alterations in a region that included the gene implicated in the hereditary disease xeroderma pigmentosum (XPG, also known as Ercc5). Complementation with wild-type XPG restored the drug sensitivity. Xeroderma pigmentosum cells deficient in the NER genes XPG, XPA, XPD or XPF were resistant to Et743, and sensitivity was restored by complementation with wild-type genes. Moreover, studies of cells deficient in XPC or in the genes implicated in Cockayne syndrome (CSA and CSB) indicated that the drug sensitivity is specifically dependent on the transcription-coupled pathway of NER. We found that Et743 interacts with the transcription-coupled NER machinery to induce lethal DNA strand breaks.

journal_name

Nat Med

journal_title

Nature medicine

authors

Takebayashi Y,Pourquier P,Zimonjic DB,Nakayama K,Emmert S,Ueda T,Urasaki Y,Kanzaki A,Akiyama SI,Popescu N,Kraemer KH,Pommier Y

doi

10.1038/91008

keywords:

subject

Has Abstract

pub_date

2001-08-01 00:00:00

pages

961-6

issue

8

eissn

1078-8956

issn

1546-170X

pii

91008

journal_volume

7

pub_type

杂志文章

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