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作 者:李宏慧[1] 任婉丽[1] 许崇文[1] 戴皓 刘俊松[1] 汪世洋 邵渊[1] 孔莺 Shiyang;Shao Yuan;Kong Ying(Department of Otorhinolaryngology Head and Neck Surgery,the First Affiliated Hospital of Xi'an Jiaotong University,Shaanxi Xi'an 710061,China;Department of Oncology,the First Affiliated Hospital of Xi'an Jiaotong University,Shaanxi Xi'an 710061,China.)
机构地区:[1]西安交通大学第一附属医院耳鼻咽喉头颈外科,陕西西安710061 [2]西安交通大学第一附属医院肿瘤科,陕西西安710061
出 处:《现代肿瘤医学》2019年第23期4139-4144,共6页Journal of Modern Oncology
基 金:陕西省自然科学基础研究计划(面上项目)(编号:2017JM8072)
摘 要:目的:研究姜黄素对三阴性乳腺癌细胞系药物敏感性的影响及其相关机制。方法:姜黄素作用三阴性乳腺癌MDA-MB-231细胞24 h后,MTT法检测姜黄素药物毒性;应用Hoechst33342染色及FCM观察姜黄素联合表柔比星对细胞凋亡及细胞周期的影响,应用Transwell实验检测姜黄素对细胞侵袭能力的影响;应用RT-PCR、Westen blot检测姜黄素对癌基因PTN和凋亡相关基因caspase-9表达的影响。结果:姜黄素能增强表柔比星对MDA-MB-231细胞的促凋亡作用及细胞周期阻滞;Transwell结果显示姜黄素可抑制MDA-MB-231细胞侵袭,这一作用可能是通过下调PTN的表达及促进凋亡相关基因caspase-9的激活,促进了细胞的凋亡。结论:姜黄素能够通过抑制癌基因PTN的表达及上调凋亡相关基因caspase-9活性,对三阴性乳腺癌细胞起到了药物增敏作用。Objective:To investigate the drugsensitivity by curcumin on human triple-negative breast cancer cell line MDA-MB-231 and its possible mechanism in vitro.Methods:The MDA-MB-231 cells were treated with curcumin for 24 h.The MTT assay was used to evaluate the cytotoxic effects of curcumin on MDA-MB-231 cells and the impact of curcumin on the drugsensitivity was detected by apoptosis assay.The influence of curcumin combined with epirubicin on inducing apoptosis and cell cycle distribution of MDA-MB-231 were determined by Hoechst33342 staining and FCM.The expression of PTN and caspase-9 were determined by RT-PCR and Western blot.Results:The inhibitive effect of epirubicin on MDA-MB-231 cells was enhanced by curcumin.Curcumin could enhance the epirubicin inducing MDA-MB-231 cells apoptosis and promote the cell cycle arrest.Curcumin could down-regulate the expression of PTN and promote the activity of apoptosis-related gene caspase-9.Conclusion:Curcumin can enhance the drugsensitivity of the human breast cancer MDA-MB-231 cells in vitro.The mechanism may involve the cell cycle arrest and increase the apoptosis which may be associated with the suppression of PTN expression and the activity of apoptosis-related gene caspase-9.
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