lncRNA LINC01206调控银屑病角质形成细胞的功能研究

 目的探讨长链非编码RNA(lncRNA)在银屑病细胞周期信号通路中发挥的功能及其作用机制。方法 通过GEO数据库收集银屑病转录组测序数据集进行分析，筛选差异表达的基因；通过细胞信号通路富集分析（KEGG）识别调控银屑病的关键信号通路；利用加权基因共表达网络分析（WGCNA）构建lncRNA与蛋白编码基因共表达网络；通过siRNA在人永生化表皮细胞（HaCaT细胞）中敲低LINC01206，流式细胞术检测细胞周期进程。结果差异表达基因富集分析研究发现细胞周期信号通路的失调参与银屑病发病。lncRNA与蛋白编码基因共表达网络分析表明，LINC01206、LINC01269、LINC01215和LINC02159等通过与细胞周期信号通路关键基因CCNA2、CCNB1和CCNE1的相互作用调控银屑病进程。细胞实验结果显示，siRNA在HaCaT细胞中敲低LINC01206，引起细胞周期G2/M的阻滞。结论lncRNA的表达变化引起银屑病细胞周期失调，细胞周期信号通路中的关键lncRNA有望成为银屑病治疗的靶标

lncRNA LINC01206 regulates the cell cycles in psoriasis

Objective To explore the function and mechanism of lncRNA on the cell cycles in psoriasis.MethodsWe first identified the differentially expressed genes through integrative analysis of RNA seq datasets from a psoriasis cohort. Then KEGG analysis was performed to identify the key signaling pathways in psoriasis. WGCNA was used to construct the lncRNA protein coding genes (PCGs) co expression network. A specific siRNA was used to knockdown LINC01206 in HaCaT keratinocytes and the cell cycle progression was detected by flow cytometry.ResultsIntegrative analysis of RNA seq datasets from the psoriasis cohort demonstrated a dysregulation of the cell cycle pathway in psoriasis. Moreover, lncRNA protein coding gene (PCGs) co expression analysis showed that LINC01206, LINC01269, LINC01215 and LINC02159 interacted with the key factors CCNA2, CCNB1 and CCNE1, in cell cycle pathway to regulate the progress of psoriasis. Flow cytometry analysis showed that knockdown of LINC01206 induced cell cycle arrest at the G2/M phase. ConclusionsOur results demonstrate the functional mechanism of lncRNAs in the cell cycle. LncRNA may be a therapeutic target for psoriasis.