长链非编码RNA DDX11-AS1对肝癌细胞增殖、侵袭能力的影响及其机制  

Effects of lncRNA DDX11-AS1 on proliferation and metastasis of hepatocellular carcinoma and the mechanism

作　　者：羊丹 徐菁 陈保银 马竹芳 YANG Dan;XU Jing;CHEN Baoyin;MA Zhufang(3201 Hospital,Hanzhong 723000,China)

机构地区：[1]三二〇一医院,陕西汉中723000

出　　处：《山东医药》2021年第8期11-14,共4页Shandong Medical Journal

基　　金：陕西省自然科学基金项目(2018JM01054)。

摘　　要：目的观察长链非编码RNA DEAD/DEAH盒解旋酶11反义RNA1(DDX11-AS1)对肝细胞癌(HCC)细胞增殖和侵袭能力的影响,并探讨可能机制。方法采用qRT-PCR法检测HCC细胞HepG2、Huh-7、SK-hep-1及正常肝细胞LO2中的DDX11-AS1,选择DDX11-AS1表达最高的HCC细胞进行后续实验。将HCC细胞分为对照组和实验组,分别转染NC siRNA和DDX11-AS1 siRNA,采用MTS法测算细胞增殖率,平板克隆实验测算克隆形成率,Transwell实验检测细胞侵袭能力,Western blotting法检测PI3K/AKT信号通路相关蛋白。将HCC细胞分为NC组、si-DDX11-AS1组和SC79组,NC组转染NC siRNA,si-DDX11-AS1组和SC79组转染DDX11-AS1 siRNA,SC79组细胞加入PI3K/AKT信号通路激活剂SC79,NC组和si-DDX11-AS1组加入DMSO,采用MTS法测算细胞增殖率,Transwell实验检测细胞侵袭能力。结果HepG2、Huh-7、SK-hep-1细胞中DDX11-AS1表达高于LO2细胞,其中HepG2细胞DDX11-AS1表达量最高(P均<0.05)。实验组细胞增殖率、克隆形成率、穿膜细胞数及pPI3K、pAKT蛋白表达均低于对照组(P均<0.05)。SC79组、si-DDX11-AS1组细胞增殖率和穿膜细胞数低于NC组,SC79组细胞增殖率和穿膜细胞数高于si-DDX11-AS1组(P均<0.05)。结论HCC细胞中DDX11-AS1表达上调;干扰DDX11-AS1表达可抑制HCC细胞的增殖和侵袭能力,其机制可能与调控PI3K/AKT信号通路有关。Objective To study the effects of long non-coding RNA DEAD/DEAH box helicase 11(lncRNA DDX11-AS1)on the proliferation and metastasis of hepatocellular carcinoma(HCC)cells,and to explore the possible mechanism of action.Methods The qRT-PCR was used to detect the expression level of DDX11-AS1 in HCC cell lines HepG2,Huh-7,and SK-hep-1 and normal liver cell line LO2.The HCC cell line with the highest DDX11-AS1 expression was selected for the subsequent experiments.We divided HCC cells into the control group and experimental group,which were transfected with NC siRNA and DDX11-AS1 siRNA,respectively.MTS method was used to detect the proliferation ability of cells in each group,plate clone experiment was used to measure clone formation rate,Transwell test was used to detect the invasion ability,and Western blotting was used to detect the PI3K/AKT signaling pathway-related protein.We divided HCC cells into the NC group,si-DDX11-AS1 group,and SC79 group.HCC cells in the NC group were transfected with NC siRNA,si-DDX11-AS1 group and SC79 group with DDX11-AS1 siRNA,and then HCC cells in the SC79 group were added with the PI3K/AKT signaling pathway activator SC79,while the NC group and the si-DDX11-AS1 group with DMSO;the cell proliferation rate was measured by the MTS method,and the cell invasion ability was measured by the Transwell assay.Results The expression of DDX11-AS1 in HepG2,Huh-7 and SK-hep-1 cells was higher than that in LO2 cells,and the expression of DDX11-AS1 in HepG2 cells was the highest(all P<0.05).The cell proliferation rate,clone formation rate,number of transmembrane cells,pPI3K and pAKT protein expression in the experimental group were lower than those in the control group(all P<0.05).The cell proliferation rate and the number of transmembrane cells in the SC79 group and the si-DDX11-AS1 group were lower than those in the NC group,and the cell proliferation rate and the number of transmembrane cells in the SC79 group were higher than those in the si-DDX11-AS1 group(all P<0.05).Conclusion The expressio

关 键 词：肝细胞癌 lncRNA DDX11-AS1 细胞增殖 细胞侵袭 PI3K/AKT信号通路 

分 类 号：R735.7[医药卫生—肿瘤]