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作 者:张月林[1] 李筱俊[1] 叶云[1] 王秀[1] 祝晓光[1]
机构地区:[1]安徽蚌埠医学院药理教研室,安徽蚌埠233030
出 处:《癌变.畸变.突变》2008年第2期96-99,共4页Carcinogenesis,Teratogenesis & Mutagenesis
基 金:安徽省教育厅自然科学重点研究项目(2005KJ047ZD)
摘 要:背景与目的:探讨赖氨匹林(Aspisol)在抑制人乳腺癌MCF_7细胞增殖过程中,对ERK1/2MAPK信号转导通路的影响。材料与方法:采用免疫细胞化学方法测定MCF_7细胞中环氧合酶_2(COX_2)的表达。采用噻唑蓝(MTT)比色法检测Aspisol对MCF_7增殖的抑制作用;采用流式细胞仪检测细胞凋亡情况;应用Westernblot分别检测ERK1/2、p_ERK1/2蛋白和凋亡相关蛋白Bcl_2、Bax的表达。结果:在MCF_7细胞中未检测到COX_2的表达。Aspisol对MCF_7细胞增殖有明显的抑制作用,且具有剂量和时间依赖性(P<0.01)。Aspisol可诱导MCF_7细胞凋亡,并随着剂量的增大细胞的凋亡率升高(P<0.05)。Aspisol抑制MCF_7细胞p_ERK蛋白的表达(P<0.05),但不影响总ERK1/2蛋白的表达(P>0.05);Aspisol可促进Bax蛋白表达(P<0.05),但抑制Bcl_2的表达(P<0.05)。结论:Aspisol影响ERK1/2MAPK信号转导通路,调节凋亡相关蛋白表达是其抑制MCF_7细胞增殖的作用之一。BACKGROUND AND AIM: To study the role of ERK1/2 MAPK signaling transduction pathway in the inhibition of MCF-7 breast cancer cells by Aspisol. MATERIALS AND METHODS: The expression of COX-2 in MCF-7 breast cancer cells was detected by immunohistochemistry.The inhibitive effects of Aspisol on MCF-7 cells were assessed with MTT assay. Apoptosis was evaluated by flow cytometry. The ERK1/2, p-ERK1/2, Bcl-2 and Bax protein expressions were measured by using Western blot method, RESULTS: The expression of COX-2 in MCF-7 cells was not found.Aspisol inhibited the proliferation of MCF-7 cells in a time- and dose-dependent manner. Aspisol also induced the apeptosis of MCF-7 cells.The protein expression of p- ERK1/2, Bcl-2 decreased and Bax increased with the dose of Aspisol but not affect total ERK1/2 expression. CONCLUSION: Aspisol could affect the ERK1/2 MAPK signaling transduction pathway and induce the expressions of apeptosis-related proteins to inhibit the proliferation of MCF-7 breast cancer cells.
关 键 词:赖氨匹林 ERK1/2 细胞凋亡 信号转导 乳腺癌细胞
分 类 号:R963[医药卫生—微生物与生化药学]
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