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目的初步筛选伴13号染色体缺失的多发性骨髓瘤患者CD138+细胞差异表达显著的microRNAs(miRNAs)并探求其生物学功能。方法通过荧光原位杂交(FISH)实验从29例多发性骨髓瘤初治患者中筛选出13号染色体缺失和核型正常的多发性骨髓瘤患者各3例;应用miRNA芯片技术获得差异表达miRNAs,并进行实时定量PCR验证;应用在线软件预测差异miRNAs的潜在靶基因,并建立miRNAs与靶基因的调控网络。结果检测出5个在伴13号染色体缺失的多发性骨髓瘤患者CD138+细胞中差异表达的miRNAs,其中4个表达下调,1个表达上调;生物信息学分析显示,SMAD3基因位于miRNAs-靶基因调控网络的关键节点上。结论伴13号染色体缺失的多发性骨髓瘤患者CD138+细胞中存在特异性表达的miRNAs;SMAD3基因可能在该类型多发性骨髓瘤发病中发挥作用。
Objective To screen differentially expressed microRNAs (miRNAs) of CD138 + cells in patients with multiple myeloma with chromosome 13 deletion and explore their biological functions. Methods Three patients with multiple myeloma with chromosome 13 deletion and normal karyotype were selected from 29 patients with multiple myeloma by fluorescence in situ hybridization (FISH). MiRNAs were differentially expressed using miRNA microarray. Real-time quantitative PCR was used to validate the potential target genes of different miRNAs by online software, and the regulatory networks of miRNAs and target genes were established. Results Five differentially expressed miRNAs were detected in CD138 + cells in patients with multiple myeloma with deletion of chromosome 13, of which four were down-regulated and one was up-regulated. Bioinformatics analysis showed that SMAD3 was located in the miRNAs- On the key nodes of the network. Conclusion There are miRNAs specifically expressed in CD138 + cells in patients with multiple myeloma with chromosome 13 deletion. SMAD3 gene may play a role in the pathogenesis of multiple myeloma.