Anti-tumor Effect of Piceatannol on Triple Negative Breast Cancer Cell Line MDA-MB-468 and Its Mechanism
10.13422/j.cnki.syfjx.20202422
- VernacularTitle:白皮杉醇对三阴性乳腺癌细胞系MDA-MB-468抗肿瘤作用及机制
- Author:
Feng-xian WANG
1
;
Shi-hua YE
2
;
Zhuo-jia ZHAO
2
;
Wei XIE
2
;
Jin WANG
2
Author Information
1. Graduate School，Shanghai University of Traditional Chinese Medicine，Shanghai 201203，China
2. School of Pharmacy， Shanghai University of Medicine and Health Sciences，Shanghai 201318，China
- Publication Type:Research Article
- Keywords:
piceatannol;
triple negative breast cancer;
Wnt/β-catenin signaling pathway;
MDA-MB-468 cells;
apoptosis
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2021;27(7):42-48
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of piceatannol （PIC） on the proliferation， apoptosis and cell cycle of MDA-MB-468 triple negative breast cancer cells and its mechanism. Method:The methylthiazolyldiphenyl-tetrazoliu bromide （MTT） colcorimetry method was used to investigate the effect of different concentrations of PIC （0， 2.5， 5.0， 10.0， 20.0， 40.0， 80.0， 160.0 μmol·L-1） on the cell viabilities of triple negative breast cancer MDA-MB-468 cells and calculate the half maximal inhibitory concentration （IC50） value， the effect of different concentrations of PIC （5.0， 10.0， 20.0 μmol·L-1） on the cell cycle of MDA-MB-468 were investigated by flow cytometry with propidium iodide （PI） staining. The apoptotic effect of PIC （5.0， 10.0， 20.0 μmol·L-1） on MDA-MB-468 cells in triple negative breast cancer was investigated by flow cytometry with cell apoptosis detection Annexin V-FITC and PI double staining. Western blot was used to investigate the effect of different concentrations of PIC （5.0， 10.0， 20.0 μmol·L-1） on the proliferation and apoptosis of MDA-MB-468 cells and detect the expressions ofsecreted glycoprotein Wnt/β-catenin pathway related proteins. Result:MTT results showed that compared with the blank group， PIC could inhibit the proliferation of MDA-MB-468 cells in a concentration-dependent manner （P<0.05， P<0.01）， with IC50 at（39.4±4.6）μmol·L-1. Compared with the blank group， PIC could increase the percentage of MDA-MB-468 cells in G0/G1 phase about cell cycle in a concentration-dependent manner （P<0.01）. Compared with the blank group， 5.0， 10.0， 20.0 μmol·L-1 PIC could induce apoptosis of MDA-MB-468 cells for 48 h（P<0.01）， and the apoptosis rate of MDA-MB-468 cells reached 49.87% when treated with 20.0 μmol·L-1 for 48 h. Compared with the blank group， PIC could significantly reduce the expressions of β-catenin， proto-oncogene （C-myc） and adhesion factor （CD44） proteins in MDA-MB-468 cells， significantly inhibit the phosphorylation of protein kinase B （Akt） and p38 mitogen activated protein kinase （p38 MAPK） proteins and the protein expression of B lymphocyte tumor-2 （Bcl-2）， and enhance cysteine aspartic acid protease-3 （Caspase-3）， Bcl-2 related X protein （Bax） and phosphorylated β-catenin protein expression（P<0.01）. Conclusion:PIC may inhibit the proliferation of MDA-MB-468 cells by inhibiting the Wnt/β-catenin signaling pathway， block the cell cycle in G0/G1 phase， and induce its apoptosis.
