Recurrent genome copy number aberrations are known to be a common feature of many cancers,including hepatocellular carcinoma(HCC),and their analysis is expected to reveal genes involved in carcinogenesis.Genome copy number variation(CNV)is one of the mechanisms to regulate the expression level of genes which contributes to the development and progression of cancer.However,in many regions with high frequency copy number variations(CNVs),the aberrantly expressed protein-coding genes is unable to make a sense,which suggests that the mechanisms underlying carcinogenesis may be partly contributed to the differently expression of long non-coding RNAs(IncRNAs).We carried out an association analysis of lncRNAs expression microarray and genome copy number variations data in HCC was and identified a set of lncRNAs whose expression levels correlated with common chromosomal aberrations.Then we examined the relative copy number and expression levels of the related lncRNAs at candidate regions in 42 pairs HBV-related HCC and paired adjacent nontumor tissues via real-time quantitative PCR methods.Among these lncRNA-PRAL(P53 Regulatory Associated LncRNA)is consistently decreased(p<0.001,n=42)with a significant correlation with the copy number variations(R=0.537,p=0.006).We further found that IncRNA-PRAL could promote the tumor cell apoptosis and suppress the progress of carcinogenesis in vivo.Moreover,lncRNA-PRAL can participate in HSP90-p53 protein complex formation to help facilitate the nuclear transportation of p53.A large amount of regions of high frequent copy number variations can be ascribed to the lncRNAs genome aberrations.And lncRNA-PRAL can promotes the tumor cell apoptosis through p53 and it presents this functional copy-number variation as a potential therapeutic target for HCC.