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作 者:林辉[1] 周懿[1] 周燚 李慧芬 杨远[2] 侯克柱[1] Lin Hui;Zhou Yi;Zhou Yi;Li Huifen;Yang Yuan;Hou Kezhu(First Department of Surgery,Shidong Hospital of Yangpu District in Shanghai,Shanghai,200438,China.;Third Department of Hepatic Surgery,Eastern Hepatobiliary Surgery Hospital,Second Military Medical University,Shanghai 200433,China.)
机构地区:[1]上海市杨浦区市东医院普外一科,上海200438 [2]第二军医大学东方肝胆外科医院肝外三科,上海200433
出 处:《贵州医药》2020年第2期171-174,共4页Guizhou Medical Journal
基 金:上海市杨浦区科学技术委员会及卫生和计划生育委员会立项资助(YP18M05);上海市杨浦区卫生和健康委员会“好医师”建设工程;国家自然科学基金创新研究群体(81521091);国家人类资源平台(2005DKA21300)。
摘 要:目的研究miR-301b-3p在肝细胞癌中的表达情况及其对肝癌细胞增殖的影响。方法采用qRT-PCR检测miR-301b-3p在肝癌组织和细胞系中的表达情况。采用免疫印迹法和荧光素酶报告子法研究miR-301b-3p与SATB2蛋白的相互作用关系。采用CCK8实验评估细胞的增殖能力。结果在本研究中,qRT-PCR结果证实miR-301b-3p在HCC组织和肝癌细胞系中下调表达。将miR-301b-3p mimic转染至HepG2细胞后,HepG2细胞的增殖能力显著被抑制。结合生物信息学分析、荧光素酶报告实验、qRT-PCR以及免疫印迹实验中证实,SATB2是miR-301b-3p在肝癌细胞中的直接作用靶点。在HepG2细胞中,miR-301b-3p抑制SATB2的mRNA和蛋白表达水平。结论本研究结果表明,miR-301b-3p通过抑制SATB2调控肝癌细胞增殖,提示miR-301b-3p可能是肝癌治疗的一个潜在的靶点。Objective To study expression of miR-301 b-3 p in hepatocellular carcinoma(HCC)and its effect on(HCC)proliferation.Methods Expression of miR-301 b-3 p in HCC tissues and cell lines was detected by qRT-PCR.A western blot assay and Luciferase reporter assay were employed to study the interaction between miR-301 b-3 p and AT-rich sequence-binding protein-2(SATB2).Cell proliferation was measured by CCK8 analyses.Results In this study it was observed low expression of the miR-301 b-3 p in both HCC tissues and hepatoma cell line as compared to normal control.Further to investigate the role of miR-301 b-3 p in HCC development,HepG2 cells were transfect with miR-301 b-3 p mimic.Following transfection,miR-301 b-3 p expression was significantly increased,which further repressed proliferation of HepG2 cells.Bioinformatics,Luciferase Reporter,and qRT-PCR,and western blotting assays indicated that special SATB2 was a direct target of miR-301 b-3 p in HCC cells.There was a negative correlation between the expression levels of SATB2 and miR-301 b-3 p in HepG2.Conclusion The results of the present study indicated that miR-301 b-3 p regulated HCC cell proliferation through inhibiting SATB2,and suggest that miR-301 b-3 p may serve as a promising target for the treatment of HCC.
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