LncRNAs在恶性肿瘤发生发展中参与调节多条信号通路，从而调节肿瘤细胞增殖、侵袭和转移。前期结果发现，miR-619-3p在肝癌组织中表达显著下调，调节细胞衰老、凋亡和增殖。P54nrb是miR-619-3p的直接作用靶点，在肝癌组织中表达较相应癌旁组织明显升高。长链非编码RNA CTBP1-AS2在肝癌组织中表达与p54nrb表达呈正相关，结合生物学信息及pull down实验证明CTBP1-AS2上有hsa-miR-619-3p的作用位点，我们推测，CTBP1-AS2可能通过发挥miR-619-3p海绵作用，促进p54nrb表达，从而促进HCC发生发展。本课题旨在利用体内外实验及裸鼠模型，明确 CTBP1-AS2是否通过抑制miR-619-3p影响p54nrb介导的细胞凋亡和细胞增殖，从而促进HCC发生，同时拟初步探索CTBP1-AS2、miR-619-3p、p54nrb的作用网络。

LncRNAs are involved in the regulation of multiple signaling pathways in the development of malignant tumors, thereby modulate tumor cell proliferation, invasion and metastasis. Our study showed that miR-619-3p was significantly down-regulated in hepatocellular carcinoma tissues and regulated cell senescence, apoptosis and proliferation. P54nrb was a direct target of miR-619-3p whose expression in liver cancerous tissue was significantly higher than the corresponding paracancerous tissue. CTBP1-AS2 expressed highly in liver cancerous tissue than paired adjacent tissue and was positively correlated with the expression of p54nrb, combining with the bioinformatic prediction and pull down assay result that miR-619-3p could interact with CTBP1-AS2, we hypothesize that CTBP1-AS2 may promote the development of HCC by acting as a miR-619-3p sponge and up-regulating p54nrb. By application of in vitro and in vivo experiments, as well as nude mice model, this study aims to determine whether CTBP1-AS2 accelerate the development of HCC by inhibiting miR-619-3p which influence p54nrb-mediated cell apoptosis and growth, as well as explore the functional network among CTBP1-AS2, miR-619-3p and p54nrb.