期刊
BIOMEDICAL JOURNAL
卷 44, 期 6, 页码 S84-S92出版社
ELSEVIER
DOI: 10.1016/j.bj.2020.07.004
关键词
Pristimerin; MDA-MB-231 cells; Epithelial-mesenchymal transition; Integrin beta 3
The study demonstrated that pristimerin inhibits tumor growth and reverts EMT by suppressing integrin beta 3, providing important insights into its potential anti-cancer effects.
Background: Pristimerin, a natural flavonoid compound, has potential anti-tumor activities. These activities have been illustrated in various cancer cell lines, including MDA-MB-231 cells. MDA-MB-231 cells are a representative mesenchymal subtype of triple negative breast cancer (MES-TNBC) cell line. Currently, the main treatment for patients with advanced MES-TNBC is cytotoxic chemotherapy. We tried to examine the role and effect of pristimerin on epithelial-mesenchymal transition (EMT) in MDA-MB-231 cells. Methods: The effects of pristimerin on the proliferation of MDA-MB-231 cells were investigated by cloning formation growth assay. In vitro transwell and adhesion assays were performed for cell invasion and adhesion. The expression levels of EMT markers in E-cadherin and N-cadherin were examined by western blotting. We also established overexpressed- and silenced-integrin beta 3 cell lines to evaluate the role of integrin beta 3 in mediating the EMT reversion events in MDA-MB-231 cells. Results: Pristimerin inhibited cell proliferation, and its inhibitory effect was dose-dependent. We demonstrated that pristimerin reserved EMT by upregulating E-cadherin and downregulating N-cadherin expression. Meanwhile, we revealed that pristimerin inhibited mRNA and protein expression of integrin beta 3, which is a key heterodimeric transmembrane receptor associated with EMT. These inhibitory effects and reversion of EMT were enhanced when integrin beta 3 was knockdown in MDA-MB-231 cells, while the overexpression of integrin overexpression of integrin beta 3 attenuated these effects. In vivo studies using xenograft3 attenuated these effects. In vivo studies using xenograft mouse model demonstrated that pristimerin inhibited tumor growth. Conclusions: Our findings provide important insights into the effects of pristimerin on inhibiting cancer progression and EMT reversion by suppression of integrin beta 3.
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