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Artemisia princeps var. orientalis induces cell cycle arrest accompanied by upregulation of p21 CIP1 and caspase‐dependent apoptosis in human breast carcinoma cells
Author(s) -
Choi EunJeong,
Kim GunHee
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1028.3
Subject(s) - apoptosis , cell cycle checkpoint , cyclin b1 , cell cycle , cyclin dependent kinase 1 , cyclin a , caspase , microbiology and biotechnology , downregulation and upregulation , cyclin e , cyclin , cell growth , cyclin d1 , mtt assay , chemistry , biology , cancer research , programmed cell death , biochemistry , gene
The aim of the present study was to investigate the anticancer activity and mechanism of action of methanol extract from Artemisia princeps var. orientalis (APME). First, the antiproliferative activity of APME against T47D cells was at various concentrations (5–200 μg/mL) and treatment times (24–72 h) determined by MTT assay. APME significantly inhibited cell proliferation in a dose‐dependent manner, regardless of treatment times. Under the same condition, cytotoxicity (LDH release) of APME was only appeared at 72 h. In addition, treatment with the IC 50 concentration of APME for 24 h caused cell cycle arrest and apoptosis. APME arrested cells in both G1 and G2/M phases of the cell cycle, a response that was related to the induction of CDK1, cyclin B, p21 Cip1 expression, and repression of CDK2 and cyclin A. The induction of p21 Cip1 by APME caused activation of p53 and modulation of its downstream targets Bcl‐2 and Bax. Subsequently, caspase‐8 and ‐9 were cleaved in cells treated with APME. Activation of these caspases in turn led to increased activation of caspase‐3. The results of this study suggest that APME produce anticancer effects in T47D cells through cell cycle arrest associated with the induction of p21 Cip1 and apoptosis mediated by p53 and caspase‐depedent pathways. This research was supported by Basic Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2012–0006811)