乙肝相关性肝癌中新基因CHCHD2的生物信息学分析

应用基因芯片技术获取以稳定转染HBx基因的肝癌细胞HepG2(HepG2-X)及非转染的肝癌细胞HepG2的差异表达的基因,利用生物信息学方法对新基因CHCHD2进行初步分析表明,该蛋白开放性读码框长456 bp,编码151个氨基酸残基,相对分子量为15.55 kD,等电点9.43,是主要定位于线粒体中的亲水性蛋白,二级结构均以α-螺旋和无规则卷曲为主要构件。同源性比较分析结果表明,其碱基序列与已经报道的其他17个物种相似性为64%-99%,且符合种属之间的进化关系。     

乙肝相关性肝癌组织BCLAF1、SETDB1表达与临床病理特征和术后预后的关系研究

目的：探讨乙肝相关性肝癌组织Bcl-2相关转录因子-1(BCLAF1)、组蛋白甲基化酶SET结构域分支型1(SETDB1)表达与临床病理特征和术后预后的关系。方法：选择2018年1至2020年6月南方医科大学珠江医院和高州市人民医院收治的127例行根治性手术切除的乙肝相关性肝癌患者,取手术切除的癌组织和旁组织,采用免疫组化法检测BCLAF1、SETDB1表达,分析BCLAF1、SETDB1表达与临床病理特征的关系。术后随访3年,Kaplan-Meier生存曲线分析BCLAF1、SETDB1不同表达患者生存差异,多因素Cox回归分析影响乙肝相关性肝癌患者预后的因素。结果：癌组织BCLAF1、SETDB1阳性表达率高于癌旁组织（P<0.05）。低分化、TNM分期Ⅲa期、门脉侵犯、淋巴结转移患者癌组织中BCLAF1、SETDB1阳性表达率高于中高分化、TNM分期Ⅰ～Ⅱ期、无门脉侵犯、无淋巴结转移患者癌组织（P<0.05）。BCLAF1阳性表达、SETDB1阳性表达乙肝相关肝癌患者3年总生存（OS）率低于BCLAF1阴性表达、SETDB1阴性表达乙肝相关肝癌患者（P<0.05...     

应用微阵列技术筛选PS1TP1基因转染细胞差异表达基因

阐明乙型肝炎病毒(HBV)前S1蛋白反式激活蛋白1(PS1TP1)的表达对于肝细胞的基因表达谱的影响。应用基因芯片技术对于pcDNA3.1()和pcDNA3.1()PS1TP1分别转染的HepG2细胞的基因表达谱进行分析。以肝癌细胞系HepG2基因作为模板,应用聚合酶链反应(PCR)技术扩增PS1TP1基因片段,以常规的分子生物学技术构建表达载体pcDNA3.1()PS1TP1。以脂质体技术转染肝母细胞瘤细胞系HepG2,提取总RNA,逆转录为cDNA,与转染空白表达载体pcDNA3.1()的HepG2细胞进行DNA芯片分析并比较。在4096个基因表达谱的筛选中,发现有8个基因表达水平显著上调,14个基因表达水平显著下调。PS1TP1基因的表达对于肝细胞基因表达谱有显著影响。DNA芯片技术是分析反式调节靶基因的有效技术途径。     

应用微阵列技术筛选PS1TP1基因转染细胞差异表达基因

阐明乙型肝炎病毒(HBV)前-S1蛋白反式激活蛋白1(PS1TP1)的表达对于肝细胞的基因表达谱的影响.应用基因芯片技术对于pcDNA3.1(-)和pcDNA3.1(-)-PS1TP1分别转染的HepG2细胞的基因表达谱进行分析.以肝癌细胞系HepG2基因作为模板,应用聚合酶链反应(PCR)技术扩增PS1TP1基因片段,以常规的分子生物学技术构建表达载体pcDNA3.1(-)-PS1TP1.以脂质体技术转染肝母细胞瘤细胞系HepG2,提取总RNA,逆转录为cDNA,与转染空白表达载体pcDNA3.1(-)的HepG2细胞进行DNA芯片分析并比较.在4096个基因表达谱的筛选中,发现有8个基因表达水平显著上调,14个基因表达水平显著下调.PS1TP1基因的表达对于肝细胞基因表达谱有显著影响.DNA芯片技术是分析反式调节靶基因的有效技术途径.     

胆固醇结石患者肝脏LCRα基因的蛋白差异表达及意义

目的:研究胆囊胆固醇结石患者肝脏的核受体基因:肝脏x受体a(liver Xreceptor a,LXRα)、法尼醇受体(famesoid Xreceptor,FXR)、人类固醇异生物受体(steroid xenobiotic receptor,SXR)及肝受体同类物1(liver receptor homolog-1,LRH-1)的蛋白表达,探讨胆固醇结石病的发病机理.方法:23例胆囊胆固醇结石患者(胆石组),12例无胆石症的胆囊息肉患者为对照(对照组).测定胆石胆固醇成分和胆汁脂类成分(胆固醇、磷脂和胆汁酸),并计算胆汁总脂和胆汁胆固醇饱和指数.Western-Blot法测定肝脏LRH-1、FXR、SXR及LXRa基因的蛋白表达量.结果:胆石组胆汁呈胆固醇过饱和;胆汁胆固醇摩尔百分比浓度较对照组升高,P<0.01;胆汁总脂较对照组明显下降,P<0.05;胆汁中胆汁酸和磷脂成分2组比较差异均无统计学意义(P>0.05).胆石组LRH-1蛋白表达高于对照组(0.88±0.05vs 0.69±0.03),P<0.05,LXRa、FXR和SXR表达2组差异无统计学意义(P>0.05).结论:人类肝脏LRH-1的蛋白表达增高与胆囊胆固醇结石形成有关.     

在大鼠肝癌发生过程中GABA-BR1的表达变化及意义

为探讨γ-氨基丁酸B型受体1(γ-aminobutyric acid type B1 receptor,GABA-BR1)与肝癌发生的关系,利用二乙基亚硝胺(DEN)制备诱发型大鼠肝癌模型,模拟人类肝癌发生发展过程,采用免疫组织化学技术对GABA-BR1和细胞周期素E(Cyclin E)蛋白在大鼠肝脏中的表达进行定性和定量分析.结果显示,在正常肝组织中有少量散在分布的GABA-BR1表达阳性的细胞;在变性或坏死灶周围GABA-BR1表达阳性的肝细胞较多;增生结节中部分肝细胞呈过表达;在肝癌细胞中广泛表达.Cyclin E与GABA-BR1阳性表达的细胞分布特点相似.实验结果提示,在肝癌发生发展过程GABA-BR1过表达,可能对肝细胞的异常增生或癌变过程起到抑制作用.     

乙肝病毒X蛋白通过β-catenin通路调控肝癌细胞增殖、细胞周期的研究

乙肝病毒X蛋白(HBx)是由乙型肝炎病毒(HBV)DNAX基因编码的蛋白,具有促癌作用且与乙肝相关肝癌的发生有关,但其发挥促癌作用的机制尚不清楚.在乙肝相关肝癌中,β-连环蛋白(β-catenin)通路过度激活并介导了促进细胞增殖、加速细胞周期的效应.为了观察HBx是否通过β-catenin通路调控肝癌细胞增殖、细胞周期,本实验培养肝癌Huh7细胞株并分为对照组、转染HBx质粒的HBx组、转染HBx并用β-catenin抑制剂ICG-001处理的HBx+ICG-001组、转染HBx并用β-catenin抑制剂XAV939处理的HBx+XAV939组,检测细胞增殖活力OD490nm、细胞周期及生存素(survivin)、B淋巴细胞瘤-2基因(Bcl-2)、细胞周期蛋白D1(CyclinD1)、c-myc、β-catenin、磷酸型GSK-3β(p-GSK-3β)的表达量.结果显示,HBx组的OD490nm水平、细胞周期S期、G2/M期的比例、survivin、bcl-2、cyclinD1、c-myc、β-catenin、p-GSK-3β的表达量均高于对照组,细胞周期G0/G1期的比例低于对照组(P＜0.05);HBx+ICG-001 组、HBx+XAV939组的OD490nm水平、细胞周期S期、G2/M期的比例、survivin、bcl-2、cyclinD1、c-myc、β-catenin、p-GSK-3β的表达量均低于HBx组,细胞周期G0/G1期的比例高于HBx组(P＜0.05).结果表明,HBx促进肝癌细胞增殖、加速细胞周期的作用与激活β-catenin通路有关.本研究的创新之处在于阐明HBx促进肝癌细胞增殖、加速细胞周期的分子机制,激活β-catenin通路是介导HBx上述作用的分子机制之一,这也为今后乙肝相关肝癌的防治提供了新思路、新靶点.     

肝癌中高表达基因fup1的克隆及其功能

原发性肝细胞癌是我国高发的恶性肿瘤之一，开展肝癌相关基因的研究具有重要的意义。从已经获得的在肝癌和正常肝对照中表达量有明显差异的EST片段入手，克隆了一个功能未报道的而可能与肝癌相关的基因。暂命名为fup1，该基因编码区全长1233bp，其产物的分子量约为46kD，等电点为5.48,可能是一个核蛋白。Northern 迹结果表明该基因在人类除心脏以外的多种正常组织中表达量很小，说明其分布具有一定的组织特异性，将整合有该基因的真核表达载体转染NIH3T3细胞后，MTT检测结果证明该基因的产物可能对细胞的增殖具有促进作用。     

下调窖蛋白-1表达抑制小鼠肝癌H22细胞侵袭能力

窖蛋白-1在不同肿瘤中发挥作用不同. 本研究以小鼠肝癌细胞H22为研究对象 ,观察下调窖蛋白-1表达对H22细胞侵袭能力的影响,并探讨其可能的分子机制. 利用RT－PCR和Western印迹法检测了窖蛋白-1在H22及小鼠正常肝细胞IAR20中的 表达.结果显示,窖蛋白 1在H22中的表达高于其在IAR20中的表达,提示窖蛋白 -1高表达可能与H22细胞恶性表型有关. RNA干扰和凝集素印记实验结果显示,窖 蛋白-1－siRNA能够有效抑制窖蛋白－1mRNA和蛋白表达,并抑制细胞表面N－聚糖 β1,6GlcNAc分支形成. Transwell细胞迁移和侵袭实验结果显示,与未转染组和 siRNA 对照组比较,转染窖蛋白-1 siRNA的H22细胞迁移和侵袭数目明显减少. 本研究证明,下调窖蛋白－1表达可抑制H22细胞表面N 聚糖β1,6GlcNAc分支形 成,从而抑制细胞迁移和侵袭能力.     

肝X受体激动剂通过上调NPC1基因的表达减轻apoE基因敲除小鼠动脉粥样硬化病变程度

本文研究肝X受体（LXR）激动剂对apoE基因敲除小鼠NPC1表达的影响．52只雄性apoE基因敲除小鼠被随机分成4组：（a）基础组（baseline group,n=10）;（b）对照组（control group,n=14）;（c）LXR激动剂治疗组（treatment group,n=14）;（d）LXR激动剂预防组（prevention group,n=14）．各组小鼠均被给予高脂／高胆固醇饲料喂养;基础组小鼠被赋形剂灌胃处理8周;对照组小鼠被赋形剂灌胃处理14周;LXR激动剂治疗组小鼠在前8周被赋形剂灌胃处理,后6周被T0901317灌胃处理;LXR激动剂预防组小鼠被T0901317灌胃处理14周．采用实时定量PCR,Western blot和免疫组织化学方法分别检测组织中NPC1 mRNA和蛋白质的表达;采用酶法测定血清中总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、载脂蛋白A—I（ApoA—I）和载脂蛋白B（ApoB）含量．另外,我们采用RNA干扰技术沉默人THP-1巨噬细胞NPC1基因表达,并将细胞诱导成泡沫细胞,检测T0901317对该细胞胆固醇流出的影响．结果显示,LXR激动剂治疗组和预防组小鼠的血浆TC,TG,HDL-C和ApoA．I水平都较对照组明显增高（P〈0．05）;LXR激动剂治疗组和预防组小鼠的主动脉粥样硬化斑块和脂质条纹明显少于对照组（P〈0．05）,其中治疗组减少了58.3％,预防组减少了64．2％;LXR激动剂治疗组和预防组小鼠的小肠组织、肝脏组织和主动脉NPC1表达上调（P〈0.05）;和正常THP-1巨噬细胞源性泡沫细胞比较,RNA干扰组胆固醇流出明显减少,T0901317处理组胆固醇流出明显增加,总之,LXR激动剂T0901317能减轻高脂高胆固醇饲料喂养的apoE基因敲除小鼠动脉粥样硬化病变程度并上调肝脏组织、小肠组织和主动脉NPC1的表达,NPC1基因沉默能使细胞胆固醇流出减少。     

Hepatitis B virus X protein upregulates alpha-fetoprotein to promote hepatocellular carcinoma by targeting miR-1236 and miR-329

Hepatitis B virus (HBV) infection is the most common cause of hepatocellular carcinoma (HCC) worldwide, wherein the expression of alpha-fetoprotein (AFP) is reactivated to promote tumorgenesis. Hepatitis B virus X protein (HBx) protein encoded by the HBV virus X gene has been considered to be oncogenic and implicated in hepatocarcinogenesis. However, the relationship between HBx and abnormal AFP expression in HCC is yet to be fully understood. To explore the potential regulation of HBx on AFP re-expression in HCC, 97 HCC samples of different etiologies were analyzed, and extremely higher serum AFP levels were found in patients with HBsAg⁺. Analyses of HBV-related HCC specimens showed that the expression of AFP was negatively correlated with the levels of miR-1236 and miR-329. Further analyses indicated that HBx promotes the expression of AFP by orchestrating the levels of miR-1236 and miR-329 both in vitro and in vivo. Specifically, miR-1236 and miR-329 bind to the potential target sequences in AFP mRNA 3′-untranslated region to suppress its expression. HBx transfection resulted in the significant decrement of these microRNAs and increment of AFP expression. Moreover, AFP promotes the proliferation of hepatoma cells and attenuates the proapoptotic effect of chemotherapy agents. These findings revealed a novel regulatory mechanism of HBx on the abnormal AFP expression in HCC, which may provide a therapeutic approach for combating HBV-related HCC by targeting the regulation of AFP expression.     

Polymorphism analyses of hepatitis B virus X gene in hepatocellular carcinoma patients from southern China

Chronic hepatitis B virus(HBV)infection is one of the major causes of hepatocellularcarcinoma(HCC),and the HBV X(HBx)gene plays a critical role in the molecular pathogenesis ofHBV-related HCC.We have investigated whether there are particular HBx gene mutations associated withHCC in patients from southern China.The HBx gene was examined in 51 paraffin-embedded tumor tissuesamples from patients with HCC and 25 serum samples from the HBV carrier by nested polymerase chainreaction(PCR),single-stranded conformational polymorphism and heteroduplex analysis.The HBx geneswith potentially important mutations from tumor tissue samples were cloned,sequenced and aligned withthe published HBx gene sequence.HBV genotypes in tumor tissue samples were analyzed by nested PCR.Analyses of HBx gene polymorphism showed that 31.3% of HBx gene fragments in tumor tissue sampleshad a special pattern.A common deletion at nt 382-400 of the HBx gene accompanied by 29 point mutationswas detected in four randomly selected tumor tissue samples with this pattern which caused a frame-shiftin the HBx open reading frame with a new stop codon at nt 1818,resulting in an HBx polypeptide chaintruncated at the C end in these cases.Among the four randomly selected samples,three were HBV genotypeB,and one was not detected by our present assay.In another tumor tissue sample,amplification of thefull-length HBx gene yielded a shorter fragment.Sequencing of this fragment revealed a 264 bp deletionbetween nt 1577 and 1840 of the HBV gene.These results suggest that HBx gene mutation occurs frequentlyin HCC samples,and the deletion at nt 382-400 of the HBx gene might play a role in carcinogenesis of HCCin southern China.     

Genetic and epigenetic alterations in hepatitis B virus-associated hepatocellular carcinoma

Hepatitis B virus(HBV) is a major cause of hepatocellular carcinoma(HCC). Its chronic infection can lead to chronic liver inflammation and the accumulation of genetic alterations to result in the oncogenic transformation of hepatocytes. HBV can also sensitize hepatocytes to oncogenic transformation by causing genetic and epigenetic changes of the host chromosomes. HBV DNA can insert into host chromosomes and recent large-scale whole-genome sequencing studies revealed recurrent HBV DNA integrations sites that may play important roles in the initiation of hepatocellular carcinogenesis. HBV can also cause epigenetic changes by altering the methylation status of cellular DNA, the post-translational modification of histones, and the expression of micro RNAs. These changes can also lead to the eventual hepatocellular transformation. These recent findings on the genetic and epigenetic alterations of the host chromosomes induced by HBV opened a new avenue for the development of novel diagnosis and treatments for HBV-induced HCC.     

Analysis of hepatocellular carcinoma associated with hepatitis B virus

The hepatitis B virus (HBV) is considered one of the main driving forces in the development of hepatocellular carcinoma (HCC). Human HBV is a partially double-stranded DNA (dsDNA) virus consisting of approximately 3.2 kbp. HBV predominantly infects hepatocytes via the receptor sodium taurocholate cotransporting polypeptide (NTCP) and coreceptor hepatic proteoglycan. The replication of HBV in hepatocytes leads to apoptosis while simultaneously leading to cirrhosis and cancer. Although the integration of dsDNA into the hepatocyte genome seems to be the main cause of mutation, since the discovery of their function, viral proteins have been shown to regulate the P53 pathway or P13K/AKT pathway to prevent host cell apoptosis, causing uncontrolled proliferation of liver cells leading to the formation of solid tumours. The most common treatments involve nucleo(s)tide analogue (NA) and polyethylene glycol (PEG)ylated interferon-alpha (PegIFN-α). NA treatment has been found to be effective for the majority of patients and induces few side effects. Nevertheless, the rate of seroconversion is relatively low. PegIFN treatment is contraindicated during pregnancy and leads to a higher morbidity rate, but the seroconversion rate is high. Since medicines and vaccines have been developed, the incidence and mortality of HBV related to HCC have profoundly decreased compared to those in 2000. This review investigates what can be the potential mechanism that HBV can cause HBV and the treatment used in chronic and acute infection.     

Comparison of genome-scale DNA methylation profiles in hepatocellular carcinoma by viral status

Hepatocellular carcinoma (HCC) incidence has steadily increased in the US over the past 30 years. Our understanding of epigenetic regulation in HCC is still limited, especially the impact of hepatitis B virus (HBV) or hepatitis C virus (HCV) infection on aberrant DNA methylation. We performed genome-wide DNA methylation profiling in 33 fresh frozen tumor samples, including 10 HBV-HCC, 13 HCV-HCC, and 10 non-infected (NIV-HCC) using the Illumina HumanMethylation450 BeadChip. Gene expression profiling was also performed using the Illumina whole-genome DASL HT Assay. Biological influences and gene networks of the differentially-methylated (DM) CpG loci were predicted using the Ingenuity Pathway Analysis. Genome-wide methylation analysis identified 7, 26, and 98 DM loci between HBV-HCC vs. HCV-HCC, HBV-HCC vs. NIV-HCC, and HCV-HCC vs. NIV-HCC, respectively, at P < 5 × 10^?5 for each. Overall, the DM loci were highly enriched for enhancers (48%), promoters (37%), or CpG islands and surrounding regions (37%). Most DM loci were hypermethylated in HCV-HCC compared to HBV-HCC or NIV-HCC. The DM loci were associated with a variety of biological functions including Cell Morphology (HBV-HCC vs. NIV-HCC), Cell Death/ Survival (HBV-HCC vs. NIV-HCC), or Cellular Growth and Proliferation (HCV-HCC vs. NIV-HCC). A subset of the DM loci were correlated (either positively or negatively) with their gene expression or associated with alcohol consumption, BMI, cirrhosis, diabetes, and cigarette smoking. Our findings of differential methylation by viral infection lend insights into the potential effects of viral infection on the epigenetic regulation and further the development and progression of HCC.     

Hepatitis B virus X protein inhibits autophagic degradation by impairing lysosomal maturation

Deficiency in autophagy, a lysosome-dependent cell degradation pathway, has been associated with a variety of diseases especially cancer. Recently, the activation of autophagy by hepatitis B virus X (HBx) protein, which is implicated in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC), has been identified in hepatic cells. However, the underlying mechanism and the relevance of HBx-activated autophagy to the carcinogenesis caused by HBV remain elusive. Here, by transfection of HBV genomic DNA and HBx in hepatic and hepatoma cells, we showed that HBV- or HBx-induced autophagosome formation was accompanied by unchanged MTOR (mechanistic target of rapamycin) activity and decreased degradation of LC3 and SQSTM1/p62, the typical autophagic cargo proteins. Further functional and morphological analysis indicated that HBx dramatically impaired lysosomal acidification leading to a drop in lysosomal degradative capacity and the accumulation of immature lysosomes possibly through interaction with V-ATPase affecting its lysosome targeting. Moreover, clinical specimen test showed increased SQSTM1 and immature lysosomal hydrolase CTSD (cathepsin D) in human liver tissues with chronic HBV infection and HBV-associated liver cancer. These data suggest that a repressive effect of HBx on lysosomal function is responsible for the inhibition of autophagic degradation, and this may be critical to the development of HBV-associated HCC.     

HBXIP基因对乙肝病毒X蛋白诱导细胞凋亡的影响

探讨乙型肝炎病毒X蛋白结合蛋白(hepatitisBXinteractingprotein ,HBXIP)基因在乙型肝炎病毒X蛋白(HBX)诱导肝癌细胞凋亡时对细胞周期的影响.构建HBXIP基因真核表达载体pcDNA3 hbxip ,进行瞬时基因转染,将克隆有HBx基因的pCMV X (分别为1μg、2 μg和3μg)和pcDNA3 hbxip质粒分别和共转染至人H74 0 2肝癌细胞中(总体积分别为5 0 μl) .发现瞬时转染3μgpCMV X质粒后,肝癌细胞凋亡发生率为34 4 % ,肝癌细胞的细胞周期相关蛋白p2 7表达水平发生明显上调;与对照组相比,瞬时转染1μg、2 μg和3μg时,细胞周期蛋白D和细胞周期蛋白E的表达水平均发生明显上调,但随着HBX水平的增加细胞周期蛋白D和细胞周期蛋白E的表达水平发生明显下降;在稳定转染pCMV X质粒的H74 0 2 X肝癌细胞中无明显的细胞凋亡发生,研究发现p2 7的表达水平发生了明显下调,而细胞周期蛋白D和细胞周期蛋白E的表达水平发生了明显上调;当pcDNA3 hbxip质粒与pCMV X质粒进行共瞬时转染时,细胞凋亡发生率由pcDNA3质粒与pCMV X质粒共转染时的2 9 2 %下降为13 3% ,p2 7的表达水平发生了下调,但细胞周期蛋白D和细胞周期蛋白E的表达水平无明显变化.研究结果表明,瞬时转染一定剂量的x基因可导致肝癌细胞发生凋亡,细胞周期相关蛋白p2 7、细胞周期蛋白D和     

Long non‐coding RNA F11‐AS1 inhibits HBV‐related hepatocellular carcinoma progression by regulating NR1I3 via binding to microRNA‐211‐5p

Long non‐coding RNAs (lncRNAs) could regulate growth and metastasis of hepatocellular carcinoma (HCC). In this study, we aimed to investigate the mechanism of lncRNA F11‐AS1 in hepatitis B virus (HBV)–related HCC. The relation of lncRNA F11‐AS1 expression in HBV‐related HCC tissues to prognosis was analysed in silico. Stably HBV‐expressing HepG2.2.15 cells were established to explore the regulation of lncRNA F11‐AS1 by HBx protein, as well as to study the effects of overexpressed lncRNA F11‐AS1 on proliferation, migration, invasion and apoptosis in vitro. Subsequently, the underlying interactions and roles of lncRNA F11‐AS1/miR‐211‐5p/NR1I3 axis in HBV‐related HCC were investigated. Additionally, the influence of lncRNA F11‐AS1 and miR‐211‐5p on tumour growth and metastasis capacity of HepG2.2.15 cells were studied on tumour‐bearing nude mice. Poor expression of lncRNA F11‐AS1 was correlated with poor prognosis in patients with HBV‐related HCC, and its down‐regulation was caused by the HBx protein. lncRNA F11‐AS1 was proved to up‐regulate the NR1I3 expression by binding to miR‐211‐5p. Overexpression of lncRNA F11‐AS1 reduced the proliferation, migration and invasion, yet induced apoptosis of HepG2.2.15 cells in vitro, which could be abolished by overexpression of miR‐211‐5p. Additionally, either lncRNA F11‐AS1 overexpression or miR‐211‐5p inhibition attenuated the tumour growth and metastasis capacity of HepG2.2.15 cells in vivo. Collectively, lncRNA F11‐AS1 acted as a modulator of miR‐211‐5p to positively regulate the expression of NR1I3, and the lncRNA F11‐AS1/miR‐211‐5p/NR1I3 axis participated in HBV‐related HCC progression via interference with the cellular physiology of HCC.