干细胞可通过自噬的方式来维持其干性特征。肝癌干细胞（LCSCs）是导致肿瘤转移的关键因素，而长链非编码RNA（lncRNA）是其重要的调控因子。我们前期研究发现lncRNA-TINCR在肝癌转移组织来源的LCSCs中表达显著增高，且可诱导LCSCs的自噬现象发生，但它是否与如何参与肝癌的靶向性转移尚需进一步阐明。我们拟运用生物信息学、荧光素酶报告基因、蛋白芯片等技术筛选其靶基因，并采用流式细胞术、PCR Array、裸鼠肝脏原位成瘤模型、小动物活体成像等技术进行细胞学、小鼠模型和临床样本的系统研究，逐步阐明TINCR通过调控miR-93/Atg7/自噬轴，促进LCSCs的侵袭转移，导致患者预后不良的分子机理。本研究将进一步揭示肝癌发展过程中的分子机制，为阻断或延缓癌症的进展提供理论依据和新的治疗靶点。

Stem cells could maintain the stemness by autophagy. Liver cancer stem cells (LCSCs) are the key factors being responsible for the metastasis of hepatocellular carcinoma (HCC). Long chain non-coding RNA (lncRNA) is an important regulator of LCSCs. In our previous study, we found that lncRNA-TINCR was increased significantly in LCSCs from the metastatic tissues of HCC and could induce autophagy in LCSCs. However, it need to elucidate the involvement and the molecular mechanisms of TINCR in the targeted metastasis of LCSCs. We will use bioinformatics, luciferase reporter assay and protein chip to screen the target genes. Flow cytometry, PCR Array, HCC nude mouse model and in vivo imaging in small animal were adopted on LCSCs, mouse model and clinical samples to find out the molecular mechanisms of the scientific hypothesis that TINCR promotes the invasion and metastasis of LCSCs and leads to the poor prognosis of patients via miR-93/Atg7/autophagy axis. The findings are supposed to reveal the mechanism further in the development of HCC, and provide the theoretical basis and new therapeutic targets to block or delay the progression of cancer.