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Cycloartane triterpenoids from Cimicifuga yunnanensis induce apoptosis of breast cancer cells (MCF7) via p53‐dependent mitochondrial signaling pathway
Author(s) -
Fang ZhongZe,
Nian Yin,
Li Wei,
Wu JingJing,
Ge GuangBo,
Dong PeiPei,
Zhang YanYan,
Qiu MingHua,
Liu Lei,
Yang Ling
Publication year - 2011
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.3222
Subject(s) - apoptosis , programmed cell death , triterpenoid , chemistry , stereochemistry , pharmacology , biology , cancer research , biochemistry
The present study was carried out to investigate the antitumor activity of five cycloartane triterpenoids isolated from Cimicifuga yunnanensis on the breast cancer cell line MCF7 and its corresponding drug resistant subline R‐MCF7, including cimigenol‐3‐ O ‐β‐ d ‐xylopyranoside (compound 1), 25‐ O‐ acetylcimigenol‐3‐ O ‐β‐ d ‐xylopyranoside (compound 2), 25‐chlorodeoxycimigenol‐3‐ O ‐β‐ d ‐xylopyranoside (compound 3), 25‐ O ‐acetylcimigenol‐3‐ O ‐α‐ l ‐arabinopyranoside (compound 4) and 23‐ O ‐acetylcimigenol‐3‐ O ‐β‐ d ‐xylopyranoside (compound 5). The results showed that compounds 2–5 have relatively high antitumor activity on both MCF7 and R‐MCF7 cells. The involvement of apoptosis as a major cause of cycloartane triterpenoids‐induced cell death was further confirmed. The results of RT‐PCR showed that compounds 2–5 increased the expression of p53 and bax, which led to the loss of mitochondrial potential and then resulted in the activation of caspase‐7. These findings collectively demonstrated that compounds 2–5 induced apoptosis of MCF7 via p53‐dependent mitochondrial pathway. Copyright © 2010 John Wiley & Sons, Ltd.