LncRNA-SNHG3作为乳腺癌标志物及其调控机制研究

LncRNAs could regulate the expression of encoding genes through a variety of ways, which were involved in the occurrence and development of a majority of diseases including tumors. Our previous experiments showed that lncRNA SNHG3 was highly expressed in tumor tissues and sera of breast cancer (BC) patients. Moreover, bioinformatics analysis and luciferase activity assay showed that S SNHG3 interacts with the RNA binding protein Lin28B. Therefore, we boldly speculated that high expression of SNHG3 in BC could inhibit the activity and function of LIN28B, thereby promoting malignant progression of BC through LIN28B downstream signaling pathway. Our study is expected to provide a new concept for exploring the pathogenesis of BC. Additionally, we will establish a detection method for SNHG3 by qRT-PCR and investigate the clinical significance of serum SNHG3 as a novel biomarker in clinical diagnosis, condition analysis, curative evaluation and prognosis judgement of BC.

LncRNAs可通过多种方式调控基因的表达，参与肿瘤等疾病的发生发展。我们前期研究表明：lncRNA SNHG3在乳腺癌（BC）患者癌组织及血清中均高表达，促进BC细胞的体内外生物学功能，且生物信息学分析及荧光素酶活性试验结果显示SNHG3和RNA结合蛋白Lin28B相互作用。因此我们大胆推测：BC中高表达的SNHG3通过对LIN28B的作用促进BC的恶性进展，研究可为BC发病分子机制探索提供新的理念。另外，本项目将建立SNHG3的qRT-PCR检测方法并探讨血清SNHG3作为新的标志物在BC临床诊断、病情分析、疗效评估和预后判断中的价值。

LncRNAs可通过多种方式调控基因的表达，参与肿瘤等疾病的发生发展。我们的研究表明：lncRNA SNHG3在乳腺癌（BC）组织及细胞中表达显著升高，其表达水平与BC进展及临床特征相关。体内外功能实验表明SNHG3促进BC细胞的增殖转移能力。机制方面，我们发现SNHG3主要分布于细胞质中，CSNK2A1是其主要靶基因。一方面，SNHG3可以作为内源性竞争RNA分子结合miR-485-5p，促进CSNK2A1表达；另一方面，SNHG3可以招募HuR蛋白提高CSNK2A1的mRNA分子的稳定性。回补实验表明BC中高表达的SNHG3通过对CSNK2A1的调控作用促进BC的恶性进展。本项目为BC的分子机制研究提供了新的理论，证明了SNHG3是BC的潜在诊治靶点。