摘要
目的:研究miR-122a对人喉癌细胞株Hep2细胞增殖、细胞周期以及相关蛋白表达量的影响。方法:人喉癌细胞株Hep2细胞分别转染miR-122a寡聚核苷酸(A组)和miR-122a inhibitor(阻遏物)(B组),同时设立阻遏物阴性对照(inhibitor negative control,miR-NC inhibitor)(C组)和空白对照(D组)。用RT-PCR、MTT法、流式细胞仪和Western blot技术评价各组细胞增殖和细胞周期的生物学特征。结果:转染miR-122a寡聚核苷酸后,Hep2细胞中miR-122a表达显著增加。同D组相比,A组细胞增殖水平明显受到抑制,miR-122a寡聚核苷酸能够有效诱导Hep-2细胞周期阻滞在G1/G0期,A组细胞分裂周期蛋白42表达水平明显下调,细胞周期调控因子蛋白CDK4及细胞周期素D1蛋白表达水平明显降低。结论:miR-122a寡聚核苷酸能够显著抑制喉癌细胞Hep2的增殖,miR-122a是潜在的人喉癌细胞基因治疗的候选靶点。
Objective： To study the effect of miR-122 a on inhibition proliferation of laryngeal carcinoma cell line Hep-2. Methods： The oligomucleotide of miR-122 a was transfected into laryngeal carcinoma cell line Hep2 cells,which were devided into three groups of A（ miR-122 a transfection）,B（ miR-122 a inhibitor）,C（ miR-122a-NC inhibitor） and group of D（ blank control）. The expression of miR-122 a was defected by RT-PCR,and relevant protein expression was evaluated by Western blot. The cell proliferation and cell cycle were determined by MTT assy and flow cytometry,respectively. Results： Compared to group D,miR-122 a expression in Hep2 cells was obviously elevated atter miR-122a-transfected. The proliferation of Hep2 cells in group A was significantly inhibited and the cell cycle arrested at G1 / G0 phase. The protein expression of CDC42 was downregulated with decreased expressions of CDK4 and cyclin D1 in group A. Conclusion： miR-122 a inhibits the proliferation activity of Hep2 cells,suggesting that miR-122 a can be taken as a potential candidate for gene therapy of laryngeal carcinoma.
作者
陈云华
于亚峰
CHEN Yun-Hua YU Ya-Feng(Department of Otolaryngology, Changshu Second People＇s Hospital, Changshu 215500, China)
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2017年第3期352-355,共4页
Chinese Journal of Immunology
