本研究旨在确定在成人急性髓系白血病（AML）中，长链非编码母源性表达基因3（lncRNA MEG3）的临床作用。利用qPCR测定了AML患者和健康供体骨髓中lncRNA MEG3的表达水平。还分析了lncRNA MEG3表达水平与临床特征之间的相关性。利用MTT测定和流式细胞术来确定lncRNA MEG3对AML细胞系细胞存活和凋亡的作用。通过西方印迹法确定了这些细胞中caspase-9，Bcl-2，MDM2和p53的表达水平。 lncRNA MEG3的表达水平在AML患者中显著下调。lncRNA MEG3的表达水平与患者总生存期呈正相关。lncRNA MEG3的上调不仅可以抑制细胞生长并促进凋亡，还可以增加caspase-9和p53的表达，并降低Bcl-2和MDM2的表达。 这些结果表明，在AML患者中lncRNA MEG3的下调可能促进肿瘤进展并影响p53-MDM2通路。

The aim was to determine the clinical role of long non coding maternally expressed gene 3 (lncRNA MEG3) in adult acute myeloid leukemia (AML).The expression levels of lncRNA MEG3 in bone marrow of AML patients and healthy donors were determined by qPCR. The correlation between expression levels of lncRNA MEG3 and clinical features was also analyzed. MTT assay and flow-cytometric assay were employed to determine the role of lncRNA MEG3 on the cell viability and apoptosis of AML cell lines. Expression levels of caspase-9, Bcl-2, MDM2, and p53 in those cells were determined by western blot.The expression levels of lncRNA MEG3 was significantly down-regulated in AML patients. Expression levels of lncRNA MEG3 were positively correlated with overall survival of patients. Up-regulation of lncRNA MEG3 could not only inhibit the cell growth and promoted apoptosis, but also increased the expression of caspase-9 and p53 and decreased the expression of Bcl-2 and MDM2.These results suggest that down-regulation of lncRNA MEG3 in AML patients might promote tumor progression and affect the p53-MDM2 pathway.