上皮间质转化（EMT）是乳腺癌转移机制中一个核心的生物学过程，大量文献及我们最近的研究证明，经典TGF-β信号通路在乳腺癌EMT及转移中发挥关键调控作用，但其下游分子和调控机制尚不完全清楚。我们最近在TGF-β诱导的乳腺癌EMT模型中对比了乳腺癌发生EMT前后的长链非编码RNA（LncRNA）表达谱，鉴定出多个可能协同调控Slug与ZEB1基因表达的LncRNA，并对其中AC026904.1及UCA1在TGF-β调控乳腺癌EMT过程中的作用进行了初步探讨。本课题拟在此基础上，深入研究TGF-β下游关键LncRNA分子AC026904.1及UCA1在转录、转录后多个层次共同调节Slug基因表达的新机制，阐明关键LncRNA在TGF-β介导的乳腺癌EMT及转移中的功能意义。这些研究可以拓展对TGF-β信号调控机制的认识，还可为乳腺癌转移的诊断、治疗、预后判断提供新的分子靶标，具有重要意义和价值

The epithelial-mesenchymal transition (EMT) has been considered to be a critical step in breast cancer metastasis. Numerous studies and our recent work demonstrate that classical TGF-β signaling pathway plays an essential role in regulating breast cancer EMT and metastasis. However, the downstream signaling and detailed molecular mechanisms are far from being completely understood. Recently, we established an EMT model of breast cancer induced by TGF-β and compared the LncRNA expression profiles between mesenchymal-like and epithelial-like MCF-7 cells. We identified several LncRNAs that could coordinately regulate the expression of Slug and ZEB1 and studied preliminarily on the role of LncRNA-AC026904.1 and UCA1 in the process of TGF-β-induced breast cancer EMT. On this basis, we aim to delve deeper into the underlying mechanism by which LncRNA-AC026904.1 and UCA1 coordinately regulate Slug expression at both transcriptional and posttranscriptional levels. Moreover, we aim to elucidate the functional roles of key LncRNAs in the process of breast cancer EMT and metastasis induced by TGF-β. Taken together, this study could expand our understanding of TGF-β signaling pathway and provide novel molecular targets for diagnosis, treatment and prognosis of metastatic breast cancer. Therefore, this research project is significant to the theoretical research and practical applications.