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作 者:邓华云[1] 杨杰[1] 赵克温[1] 黄雷[1] 廖晓东[1]
机构地区:[1]上海交通大学医学院病理生理学教研室,上海200025
出 处:《外科理论与实践》2014年第5期432-437,共6页Journal of Surgery Concepts & Practice
基 金:国家自然科学基金(81272262);国家重大科学研究计划(2012CB967003)
摘 要:目的:研究黏蛋白1(mucin1,MUC1)在食管癌发生中的作用,寻找食管癌发病的新机制。方法 :采用MUC1-siRNA和CTL-siRNA质粒转染Ec1.71细胞获得MUC1稳定沉默细胞系,分别通过MTT法、软琼脂克隆形成实验和裸小鼠移植瘤模型检测下调MUC1对鳞状上皮细胞食管癌细胞生长、克隆形成能力和体内成瘤能力的影响。结果:建立Ec1.71/MUC1-siRNA-A/B稳定沉默MUC1细胞系和Ec1.71/CTL-siRNA-A/B对照组细胞系各两株。与对照组Ec1.71/CTL-siRNA-A/B细胞系相比,MUC1沉默组Ec1.71/MUC1-siRNA-A/B细胞的生长速度显著减慢,软琼脂克隆数目明显减少,移植瘤的生长速度明显减慢、肿瘤体积更小。结论:MUC1与食管癌的形成密切相关,抑制其表达,可显著降低食管癌细胞的恶性程度。本研究为食管癌的发病机制研究和临床治疗提供了重要参考。Objective To explore the role and mechanisms of MUC 1 in the carcinogenesis of esophageal cancer. Methods Ecl.71 cells were transfected with MUCI-siRNA plasmids. The effects of MUC1 on cell proliferation, clone formation and in vivo tumorigenicity were determined by MTI" assay, soft agar clone formation assay and nude mice xenograft model, respectively. Results By screening, two cell lines stably-expressing MUCI-siRNA or CTL-siRNA were obtained and named as Ecl.71/MUCl-siRNA-A/B and Ecl.71/CTL-siRNA-A/B, respectively. The proliferation and clone formation of Ecl.71/MUCI-siRNA-A/B cells were significantly inhibited after silencing MUC1 expression when compared with the Ecl.71/CTL-siRNA-A/B cells. Moreover, MUC1 expression dramatically reduced the speed of tumor growth and decreased the tumor volume. Conclusions It is suggested that MUC1 is associated to esophageal cancer development, and supression of the expression reduced esophageal cancer malignancy dramatically. It can be a potential target for esophageal cancer therapy.
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