利用已有的三阴性乳腺癌(TNBC)组织芯片，前期研究发现雄激素受体(AR)的表达与肿瘤干性标志物CD44呈负相关，且AR阳性TNBC患者无进展生存期(PFS)优于AR阴性TNBC患者。为进一步探究AR在TNBC转移中的作用，选取3株AR阳性TNBC细胞株，运用lncRNA表达谱芯片筛选双氢睾酮处理前后差异表达的lncRNAs，qRT-PCR验证发现编号ENST00000431557的lncRNA变化趋势与芯片表达谱一致，将其命名为ARNILA，RACE法克隆ARNILA的全长转录本，ChIP实验发现AR能与ARNILA启动子区结合。生物信息学软件预测ARNILA与miR-204/211、miR-302及CD44之间存在相互调控关系。本课题重点阐明ARNILA在介导CD44表达调控中的作用及其对TNBC转移特性的影响机制，可能为临床TNBC患者治疗提供潜在的靶点。

We previously found that AR was negatively correlated with breast cancer stem cell marker CD44, and the androgen receptor (AR) positive TNBC patients showed significant better progression-fress survival (PFS) than AR negative ones with TNBC tissue arrary. To further investigate the role of AR in the metastasis of TNBC, differentially dysregulated-lncRNAs after DHT treatment on three AR positive TNBC cell lines were screened by lncRNA expression profiles. Then we found ENST00000431557 was consistent with the profile verified by qRT-PCR, which was named as Androgen Receptor Negatively Induced LncRNA (ARNILA) in our study. We cloned the full length transcript of ARNILA by RACE, and verified the binding of AR to the promoter of ARNILA by ChIP. Furthermore, the regulating mechanism between ARNILA, miR-204/211/302 and CD44 were predicted by bioinformatics tools. In this study, we will investigate the role of ARNILA in regulating CD44, and the involved mechanism in the metastasis of AR positive TNBCs, which should contribute to improve the molecular network in breast cancer and provide potential novel target for treatment of TNBC patients.