Activation of apoptosis by caspase-3-dependent specific RelB cleavage in anticancer agent-treated cancer cells: Involvement of positive feedback mechanism

Mizuki Kuboki; Ayumi Ito; Siro Simizu; Kazuo Umezawa

doi:10.1016/j.bbrc.2014.12.024

Activation of apoptosis by caspase-3-dependent specific RelB cleavage in anticancer agent-treated cancer cells: Involvement of positive feedback mechanism

Mizuki Kuboki, Ayumi Ito, Siro Simizu, Kazuo Umezawa

Department of Applied Chemistry

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

7 Citations (Scopus)

Abstract

DTCM-glutarimide (DTCM-G) is a newly found anti-inflammatory agent. In the course of experiments with lymphoma cells, we found that DTCM-G induced specific RelB cleavage. Anticancer agent vinblastine also induced the specific RelB cleavage in human fibrosarcoma HT1080 cells. The site-directed mutagenesis analysis revealed that the Asp205 site in RelB was specifically cleaved possibly by caspase-3 in vinblastine-treated HT1080 cells. Moreover, the cells stably overexpressing RelB Asp205Ala were resistant to vinblastine-induced apoptosis. Thus, the specific Asp205 cleavage of RelB by caspase-3 would be involved in the apoptosis induction by anticancer agents, which would provide the positive feedback mechanism.

Original language	English
Pages (from-to)	810-814
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	456
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2014.12.024
Publication status	Published - 2015 Jan 16

Keywords

Apoptosis
Caspase-3
DTCM-glutarimide
RelB
Vinblastine

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDGs

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

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10.1016/j.bbrc.2014.12.024

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Activation of apoptosis by caspase-3-dependent specific RelB cleavage in anticancer agent-treated cancer cells: Involvement of positive feedback mechanism. / Kuboki, Mizuki; Ito, Ayumi; Simizu, Siro et al.
In: Biochemical and Biophysical Research Communications, Vol. 456, No. 3, 16.01.2015, p. 810-814.

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

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title = "Activation of apoptosis by caspase-3-dependent specific RelB cleavage in anticancer agent-treated cancer cells: Involvement of positive feedback mechanism",

abstract = "DTCM-glutarimide (DTCM-G) is a newly found anti-inflammatory agent. In the course of experiments with lymphoma cells, we found that DTCM-G induced specific RelB cleavage. Anticancer agent vinblastine also induced the specific RelB cleavage in human fibrosarcoma HT1080 cells. The site-directed mutagenesis analysis revealed that the Asp205 site in RelB was specifically cleaved possibly by caspase-3 in vinblastine-treated HT1080 cells. Moreover, the cells stably overexpressing RelB Asp205Ala were resistant to vinblastine-induced apoptosis. Thus, the specific Asp205 cleavage of RelB by caspase-3 would be involved in the apoptosis induction by anticancer agents, which would provide the positive feedback mechanism.",

keywords = "Apoptosis, Caspase-3, DTCM-glutarimide, RelB, Vinblastine",

author = "Mizuki Kuboki and Ayumi Ito and Siro Simizu and Kazuo Umezawa",

note = "Funding Information: This work was supported financially in part by Grant-in-Aid for Scientific Research (B, 23310163 and 24310167) and (C, 26350975) from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan. This work was also supported in part by MEXT-Supported Program for the Strategic Research Foundation at Private Universities, which is for Aichi Medical University 2011–2015 (S1101027). Publisher Copyright: {\textcopyright} 2015 Elsevier Inc. All rights reserved.",

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AU - Umezawa, Kazuo

N1 - Funding Information: This work was supported financially in part by Grant-in-Aid for Scientific Research (B, 23310163 and 24310167) and (C, 26350975) from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan. This work was also supported in part by MEXT-Supported Program for the Strategic Research Foundation at Private Universities, which is for Aichi Medical University 2011–2015 (S1101027). Publisher Copyright: © 2015 Elsevier Inc. All rights reserved.

PY - 2015/1/16

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N2 - DTCM-glutarimide (DTCM-G) is a newly found anti-inflammatory agent. In the course of experiments with lymphoma cells, we found that DTCM-G induced specific RelB cleavage. Anticancer agent vinblastine also induced the specific RelB cleavage in human fibrosarcoma HT1080 cells. The site-directed mutagenesis analysis revealed that the Asp205 site in RelB was specifically cleaved possibly by caspase-3 in vinblastine-treated HT1080 cells. Moreover, the cells stably overexpressing RelB Asp205Ala were resistant to vinblastine-induced apoptosis. Thus, the specific Asp205 cleavage of RelB by caspase-3 would be involved in the apoptosis induction by anticancer agents, which would provide the positive feedback mechanism.

AB - DTCM-glutarimide (DTCM-G) is a newly found anti-inflammatory agent. In the course of experiments with lymphoma cells, we found that DTCM-G induced specific RelB cleavage. Anticancer agent vinblastine also induced the specific RelB cleavage in human fibrosarcoma HT1080 cells. The site-directed mutagenesis analysis revealed that the Asp205 site in RelB was specifically cleaved possibly by caspase-3 in vinblastine-treated HT1080 cells. Moreover, the cells stably overexpressing RelB Asp205Ala were resistant to vinblastine-induced apoptosis. Thus, the specific Asp205 cleavage of RelB by caspase-3 would be involved in the apoptosis induction by anticancer agents, which would provide the positive feedback mechanism.

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Activation of apoptosis by caspase-3-dependent specific RelB cleavage in anticancer agent-treated cancer cells: Involvement of positive feedback mechanism

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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