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Fangchinoline Induces G1 Arrest in Breast Cancer Cells Through Cell‐Cycle Regulation
Author(s) -
Xing Zhibo,
Zhang Youxue,
Zhang Xianyu,
Yang Yanmei,
Ma Yuyan,
Pang Da
Publication year - 2013
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.4936
Subject(s) - cyclin dependent kinase 6 , cyclin dependent kinase , tetrandrine , cell growth , cell cycle , cyclin dependent kinase 2 , cyclin e , cyclin d1 , cyclin dependent kinase 4 , cell cycle checkpoint , biology , palbociclib , cancer research , cancer cell , kinase , cancer , chemistry , breast cancer , pharmacology , microbiology and biotechnology , cell , biochemistry , metastatic breast cancer , genetics
Fangchinoline, an alkaloid derived from the dry roots of Stephaniae tetrandrine S. Moore (Menispermaceae), has been shown to possess cytotoxic, anti‐inflammatory, and antioxidant properties. In this study, we used Fangchinoline to inhibit breast cancer cell proliferation and to investigate its underlying molecular mechanisms. Human breast cancer cell lines, MCF‐7 and MDA‐MB‐231, were both used in this study. We found that Fangchinoline significantly decreased cell proliferation in a dose‐dependent manner and induced G1‐phase arrest in both cell lines. In addition, upon analysis of expression of cell cycle‐related proteins, we found that Fangchinoline reduced expression of cyclin D1, cyclin D3, and cyclin E, and increased expression of the cyclin‐dependent kinase (CDK) inhibitors, p21/WAF1, and p27/KIP1. Moreover, Fangchinoline also inhibited the kinase activities of CDK2, CDK4, and CDK6. These results suggest that Fangchinoline can inhibit human breast cancer cell proliferation and thus may have potential applications in cancer therapy. Copyright © 2013 John Wiley & Sons, Ltd.