Research Papers:
Arctigenin inhibits STAT3 and exhibits anticancer potential in human triple-negative breast cancer therapy
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Abstract
Tingting Feng1,2,*, Wei Cao3,*, Wanxiang Shen4, Liang Zhang1, Xinsheng Gu5, Yang Guo5, Hsiang-i Tsai4, Xuewen Liu1, Jian Li5, Jingxuan Zhang5, Shan Li5, Fuyun Wu5, Ying Liu1,5
1Laboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan, Hubei 442000, China
2School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui 230032, China
3MOE Key Laboratory of Industrial Fermentation Microbiology, College of Biotechnology, Tianjin University of Science & Technology, Tianjin 300457, China
4Graduate School at Shenzhen, Tsinghua University, Shenzhen, Guangdong 518055, China
5School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, Hubei 442000, China
*These authors contributed equally to this work
Correspondence to:
Ying Liu, email: [email protected]
Keywords: arctigenin, STAT3, triple-negative breast cancers, computational docking, taxotere
Received: May 05, 2016 Accepted: November 11, 2016 Published: November 16, 2016
ABSTRACT
Triple-negative breast cancers (TNBCs) are the most aggressive and hard-to-treat breast tumors with poor prognosis, and exploration for novel therapeutic drugs is impending. Arctigenin (Atn), a bioactive lignan isolated from seeds of Arctium lappa L, has been reported to inhibit many cancer types; however, the effect of Atn on TNBC remains unclear. In this study, we demonstrated that Atn decreased proliferation, and induced apoptosis in TNBC cells. Furthermore, we explored the underlying mechanism of Atn inhibition on TNBC cells. Computational docking and affinity assay showed that Atn bound to the SH2 domain of STAT3. Atn inhibited STAT3 binding to genomic DNA by disrupting hydrogen bond linking between DNA and STAT3. In addition, Atn augmented Taxotere®-induced TNBC cell cytotoxicity. TNBC xenograft tests also confirmed the antitumor effect of Atn in vivo. These characteristics render Atn as a promising candidate drug for further development and for designing new effective STAT3 inhibitors.
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