乳腺是哺乳动物特有的器官，其发育的过程主要受到雌激素、孕激素及催乳素等多种激素的调节。乳腺在妊娠期和哺乳期发育的核心信号通路是JAK/STAT5通路。该通路受到激素刺激激活后，磷酸化转录因子STAT5，激活下游基因。但是这一关键信号通路的下游调控机制尚未完全明确。本人的前期研究表明STAT5在乳腺发育过程中通过超级增强子控制靶基因，并且在超级增强子的靶基因中发现非编码基因。本研究拟通过探究STAT5调节的超级增强子区的Bvht-miR145a-Carmn非编码基因簇在乳腺发育中的功能，发掘乳腺发育过程中的新的分子调控机制。本研究也将为理解乳腺癌的发生发展提供理论基础。

Mammary gland is an organ that distinguishes mammals from the other animals. The development of mammary gland is precisely controlled by hormones, such as oestrogen, progesterone and prolactin. The downstream JAK/STAT5 pathway is the central signaling pathway that mediates mammary gland development during pregnancy and lactation. It is activated by hormone stimulation, phosphorylates the transcriptional factor STAT5 and activates target genes. However, the underlying molecular mechanisms of this signaling pathway is not elucidated. Previously, we demonstrated that STAT5 binds to super-enhancers (SEs) to control target genes, including non-coding ones. This study is designed to explore the roles of STAT5-bound, SE-driven non-coding gene cluster Bvht-miR145a-Carmn in mammary gland development. The goal of this study is to reveal a new molecular axis in mammary gland development and provide new insights into the development of breast cancer.