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Suh, Pann-Ghill
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G2 arrest and apoptosis by 2-amino-N-quinoline-8-yl-benzenesulfonamide (QBS), a novel cytotoxic compound

Author(s)
Kim, YHShin, KJLee, TGKim, ELee, MSRyu, SHSuh, Pann-Ghill
Issued Date
2005-05
DOI
10.1016/j.bcp.2004.12.019
URI
https://scholarworks.unist.ac.kr/handle/201301/10177
Fulltext
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=17044419485
Citation
BIOCHEMICAL PHARMACOLOGY, v.69, no.9, pp.1333 - 1341
Abstract
We screened a library of 11,000 small molecular weight chemicals, looking for compounds that affect cell viability. We have identified 2-amino-N-quinoline-8-yl-benzenesulfonamide (QBS) as a potent cytotoxic compound that induces cell cycle arrest and apoptosis. Treatment of Jurkat T cells with QBS increased the levels of cyclin B I as well as phosphorylated-cdc2, which was accompanied by reduced activity of cdc2 kinase, suggesting that QBS may induce cell cycle arrest at G2 phase. Structural analogues of QBS also exhibited similar effects on cell cycle progression and cell viability. Long-term treatment with QBS resulted in DNA fragmentation, cytochrome C release, and PARP cleavage, and an increase in the number of subdiploidy cells, indicative of cellular apoptosis. Moreover, QBS-induced apoptosis was blocked by z-VAD-fmk, a pan-caspase inhibitor. These results suggest that QBS is a novel and potent compound that induces G2 arrest and subsequent apoptosis, implicating it as a putative candidate for chemotherapy. (c) 2005 Elsevier Inc. All rights reserved.
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
ISSN
0006-2952
Keyword (Author)
library screeningquinolinesulfonamideDNA damageG2 arrestapoptosis
Keyword
CARBONIC-ANHYDRASE INHIBITORSDNA-DAMAGECELL-CYCLENUCLEAR-LOCALIZATIONANTITUMOR AGENTSASSAYSULFONAMIDESDEATHP53B1

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