乳腺癌的复发转移的分子机制研究是目前热点，而miRNAs在其中起着重要作用。我们在前期的研究中发现，miR-320a在乳腺癌组织及细胞中表达明显下调，并且miR-320a表达下调与其启动子区高甲基化密切相关。体外研究表明，miR-320a过表达显著抑制乳腺癌细胞系增殖、克隆形成、诱导细胞凋亡并引起细胞周期停滞在G1期；同时，miR-320a过表达抑制裸鼠体内成瘤。本研究基于此，将进一步研究miR-320a对乳腺癌细胞生长、血管生成及转移的影响。深入探讨miR-320a诱导乳腺癌细胞凋亡的机制；在体研究miR-320a对血管生成的影响；检测miR-320a对乳腺癌转移的影响并揭示潜在的机制；通过大样本分析，检测miR-320a与IGF1R的表达相关性，并确定miR-320a表达水平与各项病理参数的相关性。最终明确miR-320a参与乳腺癌生长转移的分子机制及预后相关性，使其成为新的分子靶标。

Breast cancer (BC) is the most common cancer among women worldwide. Previously we carried out high-throughput miRNA expression profiling of human BC, and found that miR-320a was one of the most downregulated in these tumors. In vitro assays, we found that miR-320a overexpression dramatically suppressed BC cell proliferation and colony formation, and inducing cell apoptosis and G1-phase cell-cycle arrest. We also found that miR-320a overexpression significantly inhibited tumorigenesis in vivo. We then searched for the target genes of miR-320a using TargetScan and Pictar, and identified insulin-like growth factor 1 receptor (IGF1R) is a direct target of miR-320a. On this basis, we will further investigate the effects of miR-320a-overexpression on BC cell proliferation, angiogenesis, invasion and metastasis, and reveal the potential mechanism. Our study will provide a scientific basis to find new molecular diagnostic marker and treatment targets for BC.