LNC01852通过调控Bcl-2对食管癌EC9706细胞增殖和凋亡的影响及作用机制  

Effect and mechanism of LNC01852 on proliferation and apoptosis of esophageal carcinoma cell line EC9706 by regulating Bcl-2

作　　者：李蓉蓉[1] 殷先利[1] 刘振洋[1] 杨晓琳[1] LI Rongrong;YIN Xianli;LIU Zhenyang;YANG Xiaolin(Department of Gastroenterology and Urology,Hunan Tumor Hospital,Hunan Changsha 410006,China)

机构地区：[1]湖南省肿瘤医院消化泌尿内科,湖南长沙410006

出　　处：《现代肿瘤医学》2021年第22期3889-3894,共6页Journal of Modern Oncology

摘　　要：目的:探究长链非编码RNA LNC01852对食管癌EC9706细胞增殖和凋亡的影响及其作用机制。方法:选取人食管癌细胞系EC9706、KYSE30、TE-13和人食管黏膜上皮细胞系HET-1A为研究对象,分别采用siRNA基因敲减技术、实时荧光定量聚合酶链反应(qRT-PCR)、蛋白质免疫印迹(Western blot)、MTS细胞增殖实验、克隆形成实验和流式细胞术细胞凋亡实验观察LNC01852对食管癌EC9706细胞增殖和凋亡能力以及对p53-Bcl-2/Bax凋亡信号通路标志分子mRNA和蛋白表达的影响。结果:qRT-PCR结果表明,人食管癌细胞系中LNC01852的表达较食管黏膜上皮细胞系HET-1A明显升高,差异有统计学意义(P<0.05);MTS细胞增殖实验、克隆形成实验和流式细胞术细胞凋亡实验结果表明,转染siLNC01852能够明显抑制人食管癌EC9706细胞中LNC01852的表达,同时抑制细胞的增殖能力和菌落形成能力,并促进细胞发生凋亡;此外,qRT-PCR和Western blot结果进一步证实,敲减LNC01852能够明显上调人食管癌EC9706细胞中促凋亡分子p53和Bax的mRNA和蛋白表达,同时明显抑制抗凋亡分子Bcl-2的mRNA和蛋白表达,差异有统计学意义(P<0.05)。结论:LNC01852通过介导p53-Bcl-2/Bax凋亡信号影响人食管癌细胞增殖和凋亡,提示靶向LNC01852及其下游p53-Bcl-2/Bax凋亡信号,有望为临床食管癌治疗提供新的靶点和理论依据。Objective:To investigate the effects and mechanism of long-chain non-coding RNA(LNC01852)on proliferation and apoptosis of esophageal cancer EC9706 cells.Methods:Human esophageal carcinoma cell lines EC9706,KYSE30,TE-13 and human esophageal mucosal epithelial cell lines HET-1A were selected as the study objects,respectively.siRNA gene knockdown technique,real-time fluorescence quantitative polymerase chain reaction(qRT-PCR),Western blot,MTS cell proliferation assay,colony formation assay and flow cytometry cell death assay were used to observe the effects of LNC01852 on EC9706 cell proliferation and apoptosis and the expression of p53-Bcl-2/Bax apoptosis signaling pathway markers mRNA and protein.Results:The results of qRT-PCR showed that the expression of LNC01852 in human esophageal cancer cell line was significantly higher than that in esophageal epithelial cell line HET-1A,and the difference was statistically significant(P<0.05).The results of MTS cell proliferation experiment,clone formation experiment and flow cytometry cell culture experiment showed that siLNC01852 transfection could significantly inhibit the expression of LNC01852 in human esophageal cancer EC9706 cells,and thereby inhibit cell proliferation and colony formation,and promote cell apoptosis.In addition,qRT-PCR and Western blot results further confirmed that the knockdown of LNC01852 could significantly up-regulate the mRNA and protein expressions of pro-apoptotic molecules p53 and Bax in human esophageal cancer EC9706 cells,and significantly inhibit the mRNA and protein expressions of anti-apoptotic molecules Bcl-2,with significantly statistical difference(P<0.05).Conclusion:LNC01852 affects the proliferation and apoptosis of human esophageal cancer cells by mediating the apoptosis signal of p53-Bcl-2/Bax,suggesting that the targeted apoptosis signal of LNC01852 and its downstream p53-Bcl-2/Bax is expected to provide a new target and theoretical basis for the treatment of clinical esophageal cancer.

关 键 词：LNC01852 食管癌 增殖 凋亡 作用机制 

分 类 号：R735.1[医药卫生—肿瘤]