原发性肝癌是消化系统最常见恶性肿瘤之一，其恶性程度高，进展快且易发生复发与转移，整体死亡率较高，严重威胁人类生命健康。目前针对肝癌发生发展的作用机制尚不清楚。课题组前期利用肝癌组织芯片测序、生信分析及荧光素酶实验等初步验证lncRNA HMMR-AS1及NCAPG2在肝癌组织标本中高表达。过表达NCAPG2后可促进肝癌细胞增殖及侵袭并激活STAT3及NF-κB信号通路，lncRNA HMMR-AS1可通过竞争性结合miR-188-3p并促进NCAPG2表达。接下来我们将通过荧光标记的原位杂交技术、RNA结合蛋白免疫共沉淀、质谱分析、体内动物学实验（包括转基因鼠模型）等进一步验证lncRNA HMMR-AS1/miR-188-3p/NCAPG2信号通路在肝癌发生发展中的作用并深入探讨其分子机制，评估其可否作为评估肝癌预后的独立危险因素，有望为肝癌的系统治疗提供新的治疗方向和干预手段。

Hepatocellular carcinoma (HCC)is a kind of common malignant tumor with high degree of malignity, invasive fast-growing, high incidence of recurrence, metastasis and mortality， which is the critical threat to mankind's health. However, the current mechanism of HCC growth, metastasis is still unclear. According to our earlier work, using chip sequence of liver cancer tissues, bioinformatics analysis and double luciferase assay, we confirmed lncRNA HMMR-AS1 and non-SMC condensin II complex subunit G2 (NCAPG2) is frequently upregulated in liver cancer tissues. Overexpressed NCAPG2 enhanced HCC cells proliferation, metastasis and also activated STAT3 and NF-κB pathway. Moreover, lncRNA HMMR-AS1 up-regulated NCAPG2 by competitively binding miR-188-3p.Furthermore, Fluorescence In Situ Hybridization(FISH), RNA Binding Protein Immunoprecipitation Assay(RIP), mass spectrometry and sequence analysis, in vivo animal experiments (including transgenic mouse models)are designed to investigate the role of lncRNA HMMR-AS1 /miR-188-3p/NCAPG2 pathway in HCC growth，metastasis. It is also evaluated that whether NCAPG2 or lncRNA HMMR-AS1 could be a novel marker for the prognosis of HCC and a potential therapeutic target.