The treatment role of Cyperus rotundus L. to triple-negative breast cancer cells
Author(s) -
Fukai Wang,
Xiang Song,
Shuangshuang Ma,
Chen-Yu Liu,
Xiaohui Sun,
Xinzhao Wang,
Zhaoyun Liu,
Dong Liang,
Zhiyong Yu
Publication year - 2019
Publication title -
bioscience reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.938
H-Index - 77
eISSN - 1573-4935
pISSN - 0144-8463
DOI - 10.1042/bsr20190502
Subject(s) - apoptosis , cyperus rotundus , triple negative breast cancer , cell cycle , cell growth , autophagy , phytochemical , chemistry , flow cytometry , cell , cell cycle checkpoint , biology , cancer research , microbiology and biotechnology , cancer , biochemistry , breast cancer , genetics , agronomy
Cyperus rotundus L. is widely used in Traditional Chinese Medicine and studies have reported its anticancer effect, but its chemical composition and therapy mechanism remains unknown. This research aims to analyze the chemical components of the ethanol extract of Cyperus rotundus L. (EECR), detect its treatment effects on human Triple-negative breast cancer (TNBC) cells, and elucidate possible therapy mechanisms. The chemical components of EECR were detected by the Waters UPLC combined with Bruker Q-TOF mass spectrometer (UPLC-Q-TOF-MS). The phytochemical compounds were identified by comparing the mass fragmentations of each metabolite with databases such as METLIN, HMDB, and NCBI. A total of 21 compounds were identified in EECR. MDA-MB-231 and MDA-MB-468 cells were treated with various concentrations of EECR. Cell proliferation was examined using Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell apoptosis and cell cycle were detected by flow cytometry. Apoptosis- and autophagy-related protein expression was detected by Western blot. EECR inhibits the proliferation of TNBC cells (MDA-MB-231 and MDA-MB-468) in a dose-dependent manner, which may be related to the arrest of cell cycle in G 0 /G 1 phase. It induces apoptosis by promoting the expression of BAX and inhibiting the expression of BCL-2. In addition, autophagy inhibitor 3-Methyladenine (3-MA) inhibited TNBC cells pro-survival autophagy and increased the sensitivity of EECR. The present results demonstrated that EECR has potential effects on inhibits the proliferation and induction apoptosis in TNBC.
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