乳腺癌细胞转移是导致病人死亡的主要原因，但其具体机制仍然不明确。申请人前期对33对高度侵袭转移性和非高度侵袭性的乳腺癌组织及其配对癌旁组织进行转录组测序，获得差异表达lncRNA TINCR。体内、体外实验初步发现TINCR促进乳腺癌细胞迁移与侵袭。通过测序、RNA pull-down实验初步发现TINCR可能通过HuR及miRNA上调HABP1表达，激活下游PKC通路，促进乳腺癌细胞的转移。同时，初步揭示TINCR上游可能受c-MYC调控。为证实这一假说，本项目将整合临床样本、公共数据、RNA pull-down、质谱、RIP、Luciferase reporter、ChIP、裸鼠成瘤、PET-CT等实验手段进行多角度、多层次研究，阐明TINCR通过c-MYC-TINCR-HuR/let-7 family-HABP1信号轴促进乳腺癌细胞转移的分子机制，为乳腺癌转移治疗提供靶点。

Metastasis of breast cancer cell is the major cause of death of patients. However, the specific mechanism is still in dark. Our previous study confirmed that lncRNA TINCR was differential expressed in 33 pairs of breast cancer samples with higher or lower degree of invasive abilities. Furthermore, we found that TINCR promoted metastasis of breast cancer cell in vitro and in vivo. Further studies indicate that TINCR may exhibit its function via enhancing the stability of mRNA of HABP1 via increase of HuR. Moreover, we suppose that TINCR may increase expression of HABP1 via endogenous competition of miRNA. In addition, TINCR itself can be regulated by c-MYC. To confirm this hypothesis, integration analysis of breast cancer tissues in bio bank, TCGA, RNA pull-down, mass spectrometric analysis, RIP, ChIP, PET-CT and Luciferase reporter assay would be applied to explore the potential mechanism by which TINCR enhances the metastasis of breast cancer cell, offering the new target for metastasis therapy.