Inhibition of ebracteolatain A in the proliferation of breast cancer cells by interfering with PKD1-mediated MEK/ERK and PI3K/AKT signaling pathways
10.12206/j.issn.1006-0111.201912008
- VernacularTitle:月腺大戟素A通过干扰PKD1介导的MEK/ERK和PI3K/AKT信号通路抑制乳腺癌细胞增殖的研究
- Author:
Jin ZHOU
1
;
Chengjian LI
1
;
Fuli TAN
2
;
Xinying YANG
1
;
Xiaolin ZHANG
3
;
Liang ZHAO
1
Author Information
1. Department of Pharmacy, Luodian Hospital of Baoshan District, Shanghai 201908, China.
2. Division of Pharmacology Sciences, College of Pharmaceutical Science, Guangxi Medical University, Nanning 530021, China.
3. Community Health Service Center, Youyi Street, Baoshan District, Shanghai 201999, China.
- Keywords:
breast cancer;
ebracteolatain A;
PKD1
- From:
Journal of Pharmaceutical Practice
2020;38(3):241-244
- CountryChina
- Language:Chinese
-
Abstract:
Objective Breast cancer is one of the deadliest malignancies in the world. ebracteolatain A (EA) is a kind of acetylphloroglucinol extracted from ebracteolatain. To explore the specific mechanism of EA inhibiting the proliferation of breast cancer cell MCF-7, so as to provide a new approach for the clinical treatment of breast cancer. Methods EA with different concentrations were added to breast cancer cell MCF-7 to detect changes in PKD1 protein expression. The plasmid with overexpressed PKD1 was constructed and transfected into cells, and the mRNA and protein expression levels of PKD1 were detected by real-time fluorescence quantitative PCR and Western Blot assay. CCK-8 assay was used to detect changes in cell proliferation capacity. Western Blot assay was used to detect the expression level of PKD1 and its related signaling pathways. Results EA inhibited the expression of PKD1 protein in breast cancer cells with a dose-dependent manner (P< 0.05). When transfected with the overexpressed plasmid, PKD1 was significantly increased in mRNA and protein levels (P<0.001). At the same time, PKD1 overexpression significantly reversed inhibition of EA on MCF-7 proliferation (P<0.001). It was confirmed by signaling pathway analysis that EA might affect the proliferation ability of breast cancer cells by inhibiting PKD1-mediated MEK/ERK and PI3K/AKT signaling activity (P<0.05). Conclusion EA could inhibit the proliferation of breast cancer cells by regulating PKD1-mediated MEK/ERK and PI3K/AKT signaling pathways.
