中文摘要：

目的确定miR-373-3p是否参与去甲肾上腺素对结肠癌细胞RKO细胞增殖的调控。方法将结肠癌细胞RKO分为处理组和对照组,处理组细胞培养于含有终浓度10μmol/L去甲肾上腺素的培养基中,对照组培养于正常培养基中,使用MTT法检测细胞增殖的差异。使用划痕实验观察细胞迁移,使用流式细胞术检测细胞周期。通过RT-PCR检测处理组细胞的miR-373-3p表达量。合成miR-373-3p的DNA抑制剂si-miR-373-3p,将其转染入细胞,观察其对RKO细胞增殖的影响。采用SPSS22.0对数据进行统计学分析,P〈0.05视为有统计学差异。结果 10μmol/L去甲肾上腺素促进RKO细胞的体外增殖（P〈0.05）和迁移过程。细胞周期结果显示,处理组细胞S期和G2期比例均上升。处理组细胞miR-373-3p表达量上升（P〈0.05）,转染si-miR-373-3p的RKO细胞增殖受到抑制（P〈0.05）。对转染si-miR-373-3p的细胞,去甲肾上腺素不再促进细胞增殖。结论 miR-373-3p参与了去甲肾上腺素促进的结肠癌细胞RKO的增殖过程。

英文摘要：

Objective To confirm whether miR-373-3p was involved in the regulation of norepinephrine（ NE） on RKO proliferation in vitro. Methods RKO cells were divided into NE group and control group. RKO cells were cultured in medium containing final concentration of 10 μmol / L NE in NE group and normal medium in control group. Cell proliferation was measured by MTT. Wound healing was used to observe the migration ability. Flow cytometry was adopted to analyze the change of cell cycle distribution. The level of miR-373-3p was detected by real-time PCR. The si-miR-373-3p was synthesized and then transfected into cells to observe its effect on cell proliferation. SPSS22. 0 was chosen to analyze the data,and P〈0. 05 was considered as statistically significant difference.Results The 10 μmol / L NE promoted proliferation（ P〈0. 05） and migration ability of RKO cells in vitro. In NE group,the percentage of S phase and G2 phase cells were higher than in control group,and the relative expression of miR-373-3p was up-regulated（ P〈0. 05）. The si-miR-373-3p caused a decline of cell proliferation（ P〈0. 05）. NE didn＇t promote the proliferation of RKO cells after transfected with si-miR-373-3p. Conclusion The miR-373-3p may participate in the regulation of NE on RKO cells proliferation in vitro.