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

• Published in: Biological & Pharmaceutical Bulletin 2008/01/01, Vol.31(1), pp.79-84
• Main Authors: Inaba, Hiroyuki, Nagaoka, Yasuo, Kushima, Yukihiro, Kumagai, Ayako, Matsumoto, Yoshinori, Sakaguchi, Minoru, Baba, Kimiye, Uesato, Shinichi
• Format: Article
• Language: English
• Subjects: (−)-epigallocatechin; (−)-epigallocatechin gallate; Antineoplastic Agents - pharmacology; apoptosis; Apoptosis - drug effects; Caspase 3 - metabolism; Catechin - analogs & derivatives; Catechin - pharmacology; Cell Cycle - drug effects; Cell Proliferation - drug effects; confluency; HCT116 Cells; HCT116 colorectal carcinoma cell; Humans; mitogen-activated protein kinase; Mitogen-Activated Protein Kinases - metabolism
• ISSN: 0918-6158; 1347-5215
• DOI: 10.1248/bpb.31.79

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.