| 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 |
| 投稿时间：2019-12-03 修订日期：2019-12-27 点此下载全文 |
| 引用本文：周瑾,李盛建,覃福礼,杨新颖,张晓琳,赵亮.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[J].药学实践杂志,2020,38(3):241~244,276 |
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| 基金项目:国家自然科学基金-青年项目（81303300） |
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| 中文摘要:目的 乳腺癌是世界上最致命的恶性肿瘤之一。月腺大戟素A（EA）是从中药月腺大戟中提取的乙酰间苯三酚类化合物。探讨EA抑制乳腺癌细胞MCF-7增殖的具体机制，以期为乳腺癌的临床治疗提供新的思路。方法 在乳腺癌细胞MCF-7中添加不同浓度的EA药物，检测PKD1蛋白表达水平的变化。构建PKD1的过表达质粒体并转染至细胞，用实时荧光定量PCR技术和Western Blot实验检测PKD1的mRNA和蛋白表达水平。CCK-8实验用于检测细胞增殖能力的变化。Western Blot实验用于检测PKD1介导的相关信号通路中关键蛋白的表达水平。结果 EA以剂量依赖的方式抑制乳腺癌细胞中PKD1蛋白的表达（P< 0.05）。当转染过表达质粒后，PKD1在mRNA和蛋白水平上显著升高（P< 0.001）。同时过表达PKD1显著逆转EA对MCF-7的增殖抑制作用（P<0.001）。信号通路分析证实EA通过抑制PKD1介导的MEK/ERK和PI3K/AKT信号通路活性影响乳腺癌细胞的增殖能力（P<0.05）。结论 EA通过调控PKD1介导MEK/ERK和PI3K/AKT信号通路，能够抑制乳腺癌细胞的增殖。 |
| 中文关键词:乳腺癌 月腺大戟素A PKD1 |
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| Inhibition of ebracteolatain A in the proliferation of breast cancer cells by interfering with PKD1-mediated MEK/ERK and PI3K/AKT signaling pathways |
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| 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. |
| keywords:breast cancer ebracteolatain A PKD1 |
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