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Echinomycin and a novel analogue induce apoptosis of HT-29 cells via the activation of MAP kinases pathway.

Abstract：

:Echinomycin, in typical DNA minor groove binder, had comparable efficacy compared to 5-FU in the phase II trail of colon cancer treatment. To improve echinomycin's drawback (hydrophobicity, toxicity), we synthesized the YK-2000 series (echinomycin analogues). Among these, YK-2000 had the best in vitro cytotoxicity on six different human solid cancer cell lines. Echinomycin and YK-2000 were enabled to induce the apoptosis on the HT-29 colorectal cancer cell line. The hypothesis that apoptosis in the HT-29 cell was triggered by echinomycin and YK-2000 were supported through DNA laddering, poly-(ADP-ribose) polymerase (PARP) cleavage, and flow cytometric analysis. In order to explore the signaling pathway of echinomycin and YK-2000, we examined the phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2), stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), and p38 MAP kinase. However, what the mechanism of cancer cell death would be induced by echinomycin and YK-2000 is unknown. Here, we present some evidence that one of the major apoptotic signaling pathways induced by echinomycin and YK-2000 is possibly the MAP kinases pathway in HT-29 human colon cancer cells.

journal_name

Pharmacol Res

journal_title

Pharmacological research

authors

Park JY,Park SJ,Shim KY,Lee KJ,Kim YB,Kim YH,Kim SK

doi

10.1016/j.phrs.2004.01.005

keywords:

subject

Has Abstract

pub_date

2004-08-01 00:00:00

pages

201-7

issue

2

eissn

1043-6618

issn

1096-1186

pii

S1043661804000234

journal_volume

50

pub_type

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