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Taiwanin A inhibits the proliferation of triple‐negative breast cancer cells line BT‐549
Author(s) -
Syu JiaNing,
Tang FengYao
Publication year - 2017
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.31.1_supplement.790.12
Subject(s) - triple negative breast cancer , cyclin d1 , cyclin dependent kinase 1 , cancer research , breast cancer , cyclin b1 , cell growth , apoptosis , cell cycle , protein kinase b , cancer , cyclin b , mapk/erk pathway , biology , signal transduction , medicine , microbiology and biotechnology , biochemistry
Triple‐negative breast cancer (TNBC) represents approximately 10–15% of all breast cancers and patients with TNBC always have a poor outcome compared to the other types of breast cancer. Previous studies showed that Taiwanin A could have anti‐cancer effects. However, how Taiwanin A inhibits the proliferation of triple‐negative breast cancer cells are still unknown. In this study, we investigate the anti‐breast cancer effect and the molecular mechanism of Taiwanin A. Our results show that Taiwanin A inhibited the proliferation of BT‐549 cells by the induction of cell cycle arrest and apoptosis. Taiwanin A could up‐regulate p21 and inhibited the expression of cell cycle regulatory proteins, cdc2, cyclin D1, cyclin E and CDK1/2. Taiwanin A could also down‐regulate the apoptosis regulator Bcl‐2. Additionally, Taiwanin A was able to suppression of cell survival signaling through inactivation of the Akt and ERK 1/2 signaling pathways. Moreover, Taiwanin A inhibited BT‐549 cells colony formation and showed synergetic effects with cisplatin (chemotherapeutic drug) in a dose‐dependent manner. These results showed a novel mechanism of the action of Taiwanin A against TNBC cell, suggesting it may have value for development as an anti‐breast cancer agent.