Calenduloside E 6\'-methyl ester induces apoptosis
Authors: Bora Lee, Dae Young Lee, Ki Hyun Yoo, Nam In Baek, Jong-Hwa Park, In Sik Chung

Affiliations: Department of Genetic Engineering and Graduate School of Biotechnology, Kyung Hee University, Yongin 446-701, Republic of Korea

Published online on: Tuesday, April 24, 2012

Doi: 10.3892/ol.2012.693

Pages: 22-28

The aim of the present study was to investigate the cytotoxic effect of calenduloside E 6'-methyl ester (oleanolic acid 3-O-β-D-glucuronopyranoside‑6'-methyl ester) isolated from Acanthopanax sessiliflorus fruits was investigated in CT-26 mouse colon carcinoma cells. Calenduloside E 6'-methyl ester dose-dependently inhibited the viability of CT-26 cells. Apoptosis was characterized by the detection of annexin-V and sub-G1 apoptotic cell populations, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and DNA fragmentation experiments. Results showed that the number of immunostained annexin-V-FITC and sub-G1 cells increased after treatment with calenduloside E 6'-methyl ester. Calenduloside E 6'-methyl ester also increased terminal deoxynucleotidyl transferase dUTP nick end labeled-CT-26 cells. It induced DNA fragmentation. and the cleavage of caspase-8, -9, -3 and poly ADP-ribose polymerases. In addition, calenduloside E 6'-methyl ester suppressed the volume and weight of tumors in BALB/c mice subcutaneously implanted with CT-26 cells. These results indicate that calenduloside E 6'-methyl ester induces apoptosis in CT-26 mouse colon carcinoma cells and inhibits tumor growth in a CT-26 carcinoma animal model.