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机构地区:[1]江汉大学医学院病理学与病理生理学教研室,湖北武汉430056 [2]江汉大学医学院医疗系,湖北武汉430056
出 处:《基础医学与临床》2018年第3期330-334,共5页Basic and Clinical Medicine
基 金:国家自然科学基金(81272754);武汉市青年科技晨光计划(2013071004010475)
摘 要:目的探讨miR-143通过靶向雌激素受体ER-α36介导人胃癌细胞系SGC7901的侵袭。方法通过慢病毒载体的构建及包装生成上调/下调miR-143的慢病毒LV-miR-143 up和LV-miR-143 down并感染人胃癌细胞系SGC7901,用Western blot检测ER-α36的蛋白表达水平和细胞的侵袭能力;生物信息学软件预测miR-143的靶基因;荧光素酶报告基因实验验证靶基因。结果 LV-miR-143 up与LV-miR-143 down慢病毒病毒颗粒分别感染人胃癌细胞系SGC7901,感染效率均在80%以上;上调miR-143,人胃癌细胞系SGC7901的ER-α36表达水平明显下降,侵袭能力明显降低(P<0.05),反之则增加。结论 miR-143通过靶向雌激素受体ER-α36负向调控胃癌细胞SGC7901的侵袭。Objective To investigate the effects of ER-α36 on invasion of human gastric cancer cell lines SGC7901 by miR-143. Methods Lentiviral vectors were constructed to generate up-and down-regulations of miR-143 lentiviruses( LV-miR-143 and LV-anti-miR-143,respectively).The viruses were used to infect human gastric cancer cell lines SGC7901.The ER-α36 protein expression level and the invasion of constructed cells were detected by Western blot and transwell. The target gene of miR-143 was predicted by bioinformatics tools. Luciferase reporter assay was carried out to confirm the predicted target gene. Results The infection efficiency of the lentivirus titers of LV-miR-143 and LV-anti-miR-143 were over 80% shown by the green fluorescence. The ER-α36 expression level,the cell invasion in LV-miR-21 group were significantly lower than those in LV-anti-miR-21 group( P〈 0. 05). Conclusions miR-143 plays an important role in the negative control of gastric cancer invasion by the regulation of ER-α36.
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