Involvement of caspase-3 in epigallocatechin-3-gallate-mediated apoptosis of human chondrosarcoma cells

Shabana Islam; Najmul Islam; Timothy Kermode; Brian Johnstone; Hasan Mukhtar; Roland W. Moskowitz; Victor M. Goldberg; Charles J. Malemud; Tariq M. Haqqi

doi:10.1006/bbrc.2000.2536

Involvement of caspase-3 in epigallocatechin-3-gallate-mediated apoptosis of human chondrosarcoma cells

Shabana Islam, Najmul Islam, Timothy Kermode, Brian Johnstone, Hasan Mukhtar, Roland W. Moskowitz, Victor M. Goldberg, Charles J. Malemud, Tariq M. Haqqi

Orthopaedics and Rehabilitation

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118 Scopus citations

Abstract

Green tea polyphenol-(-)epigallocatechin-3-gallate (EGCG)-is a potent chemopreventive agent in many test systems and has been shown to inhibit tumor promotion and induce apoptosis. In this study we describe a novel observation that EGCG displayed strong inhibitory effects on the proliferation and viability of HTB-94 human chondrosarcoma cells in a dose-dependent manner and induced apoptosis. Investigation of the mechanism of EGCG-induced apoptosis revealed that treatment with EGCG resulted in DNA fragmentation, induction of caspase-3/CPP32 activity, and cleavage of the death substrate poly(ADP-ribose)polymerase (PARP). Pretreatment of cells with a synthetic pan-caspase inhibitor (Z-VAD FMR) and a caspase-3-specific inhibitor (DEVD-CHO) prevented EGCG-induced PARP cleavage. The induction of apoptosis by EGCG via activation of caspase-3/CPP32-like proteases may provide a mechanistic explanation for its antitumor effects. (C) 2000 Academic Press.

Original language	English (US)
Pages (from-to)	793-797
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	270
Issue number	3
DOIs	https://doi.org/10.1006/bbrc.2000.2536
State	Published - Apr 21 2000

Keywords

Apoptosis
Caspases
Chondrosarcoma
Green tea

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1006/bbrc.2000.2536

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title = "Involvement of caspase-3 in epigallocatechin-3-gallate-mediated apoptosis of human chondrosarcoma cells",

abstract = "Green tea polyphenol-(-)epigallocatechin-3-gallate (EGCG)-is a potent chemopreventive agent in many test systems and has been shown to inhibit tumor promotion and induce apoptosis. In this study we describe a novel observation that EGCG displayed strong inhibitory effects on the proliferation and viability of HTB-94 human chondrosarcoma cells in a dose-dependent manner and induced apoptosis. Investigation of the mechanism of EGCG-induced apoptosis revealed that treatment with EGCG resulted in DNA fragmentation, induction of caspase-3/CPP32 activity, and cleavage of the death substrate poly(ADP-ribose)polymerase (PARP). Pretreatment of cells with a synthetic pan-caspase inhibitor (Z-VAD FMR) and a caspase-3-specific inhibitor (DEVD-CHO) prevented EGCG-induced PARP cleavage. The induction of apoptosis by EGCG via activation of caspase-3/CPP32-like proteases may provide a mechanistic explanation for its antitumor effects. (C) 2000 Academic Press.",

keywords = "Apoptosis, Caspases, Chondrosarcoma, Green tea",

author = "Shabana Islam and Najmul Islam and Timothy Kermode and Brian Johnstone and Hasan Mukhtar and Moskowitz, {Roland W.} and Goldberg, {Victor M.} and Malemud, {Charles J.} and Haqqi, {Tariq M.}",

note = "Funding Information: This work was supported in part by NIH Grants AR-44902, AR-20618 (NEOMAC), and AR-37726 and by an Arthritis Foundation Biomedical Science grant. S.I. was supported by NIH Training Grant AR-07505.",

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T1 - Involvement of caspase-3 in epigallocatechin-3-gallate-mediated apoptosis of human chondrosarcoma cells

AU - Islam, Shabana

AU - Islam, Najmul

AU - Kermode, Timothy

AU - Johnstone, Brian

AU - Mukhtar, Hasan

AU - Moskowitz, Roland W.

AU - Goldberg, Victor M.

AU - Malemud, Charles J.

AU - Haqqi, Tariq M.

N1 - Funding Information: This work was supported in part by NIH Grants AR-44902, AR-20618 (NEOMAC), and AR-37726 and by an Arthritis Foundation Biomedical Science grant. S.I. was supported by NIH Training Grant AR-07505.

PY - 2000/4/21

Y1 - 2000/4/21

N2 - Green tea polyphenol-(-)epigallocatechin-3-gallate (EGCG)-is a potent chemopreventive agent in many test systems and has been shown to inhibit tumor promotion and induce apoptosis. In this study we describe a novel observation that EGCG displayed strong inhibitory effects on the proliferation and viability of HTB-94 human chondrosarcoma cells in a dose-dependent manner and induced apoptosis. Investigation of the mechanism of EGCG-induced apoptosis revealed that treatment with EGCG resulted in DNA fragmentation, induction of caspase-3/CPP32 activity, and cleavage of the death substrate poly(ADP-ribose)polymerase (PARP). Pretreatment of cells with a synthetic pan-caspase inhibitor (Z-VAD FMR) and a caspase-3-specific inhibitor (DEVD-CHO) prevented EGCG-induced PARP cleavage. The induction of apoptosis by EGCG via activation of caspase-3/CPP32-like proteases may provide a mechanistic explanation for its antitumor effects. (C) 2000 Academic Press.

AB - Green tea polyphenol-(-)epigallocatechin-3-gallate (EGCG)-is a potent chemopreventive agent in many test systems and has been shown to inhibit tumor promotion and induce apoptosis. In this study we describe a novel observation that EGCG displayed strong inhibitory effects on the proliferation and viability of HTB-94 human chondrosarcoma cells in a dose-dependent manner and induced apoptosis. Investigation of the mechanism of EGCG-induced apoptosis revealed that treatment with EGCG resulted in DNA fragmentation, induction of caspase-3/CPP32 activity, and cleavage of the death substrate poly(ADP-ribose)polymerase (PARP). Pretreatment of cells with a synthetic pan-caspase inhibitor (Z-VAD FMR) and a caspase-3-specific inhibitor (DEVD-CHO) prevented EGCG-induced PARP cleavage. The induction of apoptosis by EGCG via activation of caspase-3/CPP32-like proteases may provide a mechanistic explanation for its antitumor effects. (C) 2000 Academic Press.

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Involvement of caspase-3 in epigallocatechin-3-gallate-mediated apoptosis of human chondrosarcoma cells

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