Comparative Examination of Anti-proliferative Activities of (−)-Epigallocatechin Gallate and (−)-Epigallocatechin against HCT116 Colorectal Carcinoma Cells

Hiroyuki Inaba; Yasuo Nagaoka; Yukihiro Kushima; Ayako Kumagai; Yoshinori Matsumoto; Minoru Sakaguchi; Kimiye Baba; Shinichi Uesato

doi:10.1248/bpb.31.79

Regular Articles

Comparative Examination of Anti-proliferative Activities of (−)-Epigallocatechin Gallate and (−)-Epigallocatechin against HCT116 Colorectal Carcinoma Cells

Hiroyuki Inaba, Yasuo Nagaoka, Yukihiro Kushima, Ayako Kumagai, Yoshinori Matsumoto, Minoru Sakaguchi, Kimiye Baba, Shinichi Uesato

Author information

Hiroyuki Inaba
Department of Life Science and Biotechnology, Faculty of Chemistry, Material and Bioengineering, Kansai University
Yasuo Nagaoka
Department of Life Science and Biotechnology, Faculty of Chemistry, Material and Bioengineering, Kansai University
High Technology Research Center, Kansai University
Yukihiro Kushima
Department of Life Science and Biotechnology, Faculty of Chemistry, Material and Bioengineering, Kansai University
Ayako Kumagai
Department of Life Science and Biotechnology, Faculty of Chemistry, Material and Bioengineering, Kansai University
Yoshinori Matsumoto
Department of Life Science and Biotechnology, Faculty of Chemistry, Material and Bioengineering, Kansai University
Minoru Sakaguchi
Osaka University of Pharmaceutical Sciences
Kimiye Baba
Osaka University of Pharmaceutical Sciences
Shinichi Uesato
Department of Life Science and Biotechnology, Faculty of Chemistry, Material and Bioengineering, Kansai University
High Technology Research Center, Kansai University

Keywords: HCT116 colorectal carcinoma cell, (−)-epigallocatechin gallate, (−)-epigallocatechin, confluency, apoptosis, mitogen-activated protein kinase

JOURNAL FREE ACCESS

2008 Volume 31 Issue 1 Pages 79-84

DOI https://doi.org/10.1248/bpb.31.79

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Abstract

We compared anti-proliferative activities of (−)-epigallocatechin gallate (EGCG) and (−)-epigallocatechin (EGC) against HCT116 colorectal carcinoma cells. These catechins inhibited cell growth to nearly the same extent at low cell confluency in plates. However, their inhibitory effect grew weaker as cell confluence increased, and this tendency was more conspicuous for EGC than for EGCG. Both EGCG and EGC activated the phosphorylation of the major MAPKs, ERK, JNK, and p38, in the HCT116 cells as in many other established human cancer cells though to different extents. Cell cycle analyses, DNA fragmentation assays, and TUNEL assays as well as Western blot assays suggested that these catechins inhibited cell growth through mitogen-activated protein kinase (MAPK)-mediated apoptosis rather than cell cycle regulation.

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