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Suppression of human breast cancer cells by tectorigenin through downregulation of matrix metalloproteinases and MAPK signaling in�vitro
Author(s) -
Linwen Zeng,
Shaofeng Yuan,
Jianliang Shen,
Ming Wu,
Liangming Pan,
Xiangdong Kong
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.8313
Subject(s) - protein kinase b , cell cycle , cancer research , apoptosis , biology , cell growth , mapk/erk pathway , cancer cell , pi3k/akt/mtor pathway , oncogene , cancer , chemistry , signal transduction , microbiology and biotechnology , biochemistry , genetics
Breast cancer is a major life‑threatening malignancy and is the second highest cause of mortality. The aim of the present study was to investigate the effects of tectorigenin (Tec), a Traditional Chinese Medicine, against human breast cancer cells in vitro. MDA‑MB‑231 and MCF‑7 human breast cancer cells were treated with various concentrations of Tec. Cell proliferation was evaluated using the Cell Counting kit‑8 assay, and apoptosis and the cell cycle were examined by flow cytometry. The migratory and invasive abilities of these cells were detected by Transwell and Matrigel assays, respectively. Metastasis‑, apoptosis‑ and survival‑related gene expression levels were measured by reverse transcription‑quantitative polymerase chain reaction and western blotting. The results indicated that Tec was able to inhibit the proliferation of MDA‑MB‑231 and MCF‑7 cells in a dose‑ and time‑dependent manner. Furthermore, Tec treatment induced apoptosis and G0/G1‑phase arrest, and inhibited cell migration and invasion. Tec treatment decreased the expression of matrix metalloproteinase (MMP)‑2, MMP9, BCL‑2, phosphorylated‑AKT and components of the mitogen‑activated protein kinase (MAPK) signaling pathway, and increased the expression of BCL‑2‑associated X, cleaved poly [ADP‑ribose] polymerase and cleaved caspase‑3. In conclusion, Tec treatment suppressed human breast cancer cells through the downregulation of AKT and MAPK signaling and the upregulated expression and/or activity of the caspase family in vitro. Therefore, Tec may be a potential therapeutic drug to treat human breast cancer.

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