长链非编码RNA SNHG16在胰腺癌中的表达及功能  

Expression and Function of Long-chain Non-coding RNA SNHG16 in Pancreatic Carcinoma

作　　者：王剑[1] 马松林[1] 周婷婷 廖宇圣[1] Wang Jian;Ma Songlin;Zhou Tingting(Department of Gastroenterology,The Central Hospital of Wuhan,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430014,China)

机构地区：[1]华中科技大学同济医学院附属武汉中心医院消化内科,武汉430014

出　　处：《华中科技大学学报（医学版）》2020年第1期11-16,共6页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

基　　金：武汉市科技局科研项目(No.2018404010306)。

摘　　要：目的探讨长链非编码RNA SNHG16(SNHG16)在胰腺癌中的表达及其功能。方法采用实时荧光定量PCR(qRT-PCR)法检测SNHG16在46例胰腺癌癌组织和癌旁组织中的表达。采用卡方检验分析其表达水平与临床病理参数的相关性。Kaplan-Meier生存分析比较SNHG16表达水平不同的患者生存率差异。qRT-PCR检测SNHG16在4种胰腺癌细胞系及正常胰腺导管上皮细胞系中的表达。在胰腺癌细胞系AsPC-1中敲低SNHG16表达,采用活细胞计数(CCK-8)和流式细胞术分别测定细胞增殖和凋亡水平,Transwell实验测定细胞侵袭能力,TOP/FOP闪光荧光素酶报告系统检测Wnt/β-Catenin信号激活状态,蛋白印迹法检测c-myc、β-连环蛋白(β-catenin)和细胞周期蛋白D1(cyclin D1)的表达。结果胰腺癌癌组织和细胞系中SNHG16表达显著上调(均P<0.01)。SNHG16高表达与患者肿瘤分化差、晚期TNM分期和淋巴结转移显著相关(均P<0.05)。SNHG16高表达组患者总生存率显著低于SNHG16低表达患者(P=0.003)。敲低SNHG16表达可显著抑制胰腺癌细胞增殖和侵袭能力,并促进细胞凋亡。敲低SNHG16表达可抑制Wnt/β-catenin信号通路的激活和c-myc、β-catenin和cyclin D1的表达。结论胰腺癌组织中SNHG16的表达上调,其表达水平与胰腺癌预后相关,SNHG16可能通过Wnt/β-catenin通路而促进胰腺癌细胞增殖和侵袭,并抑制凋亡,是胰腺癌潜在分子标志物。Objective To investigate the expression and function of long-chain non-coding RNA SNHG16 in pancreatic carcinoma.Methods The expression of SNHG16 in pancreatic cancer and adjacent tissues of 46 cases were detected by real-time fluorescence quantitative PCR(qRT-PCR).Chi-square test was used to analyze the correlation between the expression level and clinicopathological parameters.Kaplan-Meier survival analysis was used to compare the survival rates of patients with high and low SNHG16 expression.The expression of SNHG16 in four pancreatic cancer cell lines and normal pancreatic ductal epithelial cell lines was detected by qRT-PCR.SNHG16 expression was knocked down in pancreatic cancer cell line AsPC-1 and divided into SNHG16 knockdown expression group(si-Lnc SNHG16 group)and negative control group(si-NC group).Proliferation and apoptosis were measured by CCK-8 and flow cytometry,respectively.Invasion ability was measured by Transwell assay,and activation of Wnt/β-catenin signaling pathway was detected by TOP/FOP flash luciferase reporting system.The expression levels of c-myc,β-catenin and cyclin D1 were detected by Western blotting.Results The expression of SNHG16 was significantly up-regulated in pancreatic cancer tissues and cell lines(P<0.01).The high expression of SNHG16 was significantly correlated with poor differentiation,advanced TNM stage and lymph node metastasis(P<0.05).The overall survival rate of patients with high SNHG16 expression was significantly lower than that of patients with low SNHG16 expression(P=0.003).Knocking down the expression of Lnc SNHG16 significantly inhibited the proliferation and invasion of pancreatic cancer cells,and promoted cell apoptosis.Knocking down the expression of SNHG16 inhibited the activation of Wnt/β-catenin signaling pathway and the expression of c-myc,β-catenin and cyclin D1.Conclusion The expression of SNHG16 is up-regulated in pancreatic cancer tissues.Its expression level is related to the prognosis of pancreatic cancer.SNHG16 may promote the proliferation

关 键 词：长链非编码RNA SNHG16 胰腺癌 增殖 侵袭 

分 类 号：R735.9[医药卫生—肿瘤]