Targeting NF-κB and induction of apoptosis by novel NF-κB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) in Burkitt lymphoma cells

Noriko Kimura; Yoshitaka Miyakawa; Kanoko Kohmura; Kazuo Umezawa; Yasuo Ikeda; Masahiro Kizaki

doi:10.1016/j.leukres.2007.02.015

Targeting NF-κB and induction of apoptosis by novel NF-κB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) in Burkitt lymphoma cells

Noriko Kimura, Yoshitaka Miyakawa, Kanoko Kohmura, Kazuo Umezawa, Yasuo Ikeda, Masahiro Kizaki

School of Medicine

Research output: Contribution to journal › Article › peer-review

14 Citations (Scopus)

Abstract

A new NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), inhibited proliferation and induced apoptosis in human Burkitt lymphoma, HS-Sultan and Daudi cell lines. The activation of caspase-3 and the cleavage of caspase substrate PARP were observed after treatment with DHMEQ. The induction of apoptosis by DHMEQ was prevented by the pretreatment of Burkitt lymphoma cells with pan-caspase inhibitor, z-VAD-FMK. The expression of anti-apoptotic factors such as IAP-1 and XIAP was suppressed by DHMEQ. Phosphorylation of ERK and JNK was induced by DHMEQ. In conclusion, these results demonstrate that NF-κB might be an ideal target to develop for new anti-cancer drugs for Burkitt lymphoma.

Original language	English
Pages (from-to)	1529-1535
Number of pages	7
Journal	Leukemia Research
Volume	31
Issue number	11
DOIs	https://doi.org/10.1016/j.leukres.2007.02.015
Publication status	Published - 2007 Nov 1

Keywords

Apoptosis
Burkitt lymphoma
Caspase-3
IAP
NF-κB

ASJC Scopus subject areas

Hematology
Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.leukres.2007.02.015

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title = "Targeting NF-κB and induction of apoptosis by novel NF-κB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) in Burkitt lymphoma cells",

abstract = "A new NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), inhibited proliferation and induced apoptosis in human Burkitt lymphoma, HS-Sultan and Daudi cell lines. The activation of caspase-3 and the cleavage of caspase substrate PARP were observed after treatment with DHMEQ. The induction of apoptosis by DHMEQ was prevented by the pretreatment of Burkitt lymphoma cells with pan-caspase inhibitor, z-VAD-FMK. The expression of anti-apoptotic factors such as IAP-1 and XIAP was suppressed by DHMEQ. Phosphorylation of ERK and JNK was induced by DHMEQ. In conclusion, these results demonstrate that NF-κB might be an ideal target to develop for new anti-cancer drugs for Burkitt lymphoma.",

keywords = "Apoptosis, Burkitt lymphoma, Caspase-3, IAP, NF-κB",

author = "Noriko Kimura and Yoshitaka Miyakawa and Kanoko Kohmura and Kazuo Umezawa and Yasuo Ikeda and Masahiro Kizaki",

year = "2007",

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doi = "10.1016/j.leukres.2007.02.015",

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journal = "Leukemia Research",

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T1 - Targeting NF-κB and induction of apoptosis by novel NF-κB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) in Burkitt lymphoma cells

AU - Kimura, Noriko

AU - Miyakawa, Yoshitaka

AU - Kohmura, Kanoko

AU - Umezawa, Kazuo

AU - Ikeda, Yasuo

AU - Kizaki, Masahiro

PY - 2007/11/1

Y1 - 2007/11/1

N2 - A new NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), inhibited proliferation and induced apoptosis in human Burkitt lymphoma, HS-Sultan and Daudi cell lines. The activation of caspase-3 and the cleavage of caspase substrate PARP were observed after treatment with DHMEQ. The induction of apoptosis by DHMEQ was prevented by the pretreatment of Burkitt lymphoma cells with pan-caspase inhibitor, z-VAD-FMK. The expression of anti-apoptotic factors such as IAP-1 and XIAP was suppressed by DHMEQ. Phosphorylation of ERK and JNK was induced by DHMEQ. In conclusion, these results demonstrate that NF-κB might be an ideal target to develop for new anti-cancer drugs for Burkitt lymphoma.

AB - A new NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), inhibited proliferation and induced apoptosis in human Burkitt lymphoma, HS-Sultan and Daudi cell lines. The activation of caspase-3 and the cleavage of caspase substrate PARP were observed after treatment with DHMEQ. The induction of apoptosis by DHMEQ was prevented by the pretreatment of Burkitt lymphoma cells with pan-caspase inhibitor, z-VAD-FMK. The expression of anti-apoptotic factors such as IAP-1 and XIAP was suppressed by DHMEQ. Phosphorylation of ERK and JNK was induced by DHMEQ. In conclusion, these results demonstrate that NF-κB might be an ideal target to develop for new anti-cancer drugs for Burkitt lymphoma.

KW - Apoptosis

KW - Burkitt lymphoma

KW - Caspase-3

KW - IAP

KW - NF-κB

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JO - Leukemia Research

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ER -

Targeting NF-κB and induction of apoptosis by novel NF-κB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) in Burkitt lymphoma cells

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

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