神经胶质瘤是中枢神经系统最常见的恶性肿瘤。胶质瘤干细胞具有干细胞相似特性，与肿瘤的多种恶性表型有关，是恶性肿瘤治疗的潜在靶点，但调控胶质瘤干细胞干性的分子机制尚不明确。LncRNAs分子是非编码RNA的一种，在基因表达调控过程中发挥着重要作用。研究表明MEG3在胶质瘤干细胞中表达显著降低，与胶质瘤的发展密切相关，同时其能够协同蛋白分子调控ESCs的分化，因而MEG3可能对胶质瘤干细胞存在调控作用。本研究拟在以往研究基础上以胶质瘤干细胞为对象，分析MEG3在胶质瘤干细胞中的特异性表达，系统探讨MEG3在胶质瘤干细胞中敲减或过表达后对胶质瘤干细胞的维持、增殖和分化等细胞生物学行为的影响，进而深入研究MEG3影响胶质瘤干细胞的可能分子机制。这些研究对于深入理解胶质瘤干细胞调控的分子机制和LncRNAs的调控作用，以及建立针对LncRNAs分子的胶质瘤干细胞干预措施，具有重要的理论和实际意义。

Gliomas derived from brain glial tissue are the most common brain tumors, and frequently leads to death.Because of their infiltrating nature and high recurrence it remains difficult to cure. Recently, tumor cells with stem-cell like properties were isolated from hematological and many solid tumors, including brain tumors. This subpopulation of tumor cells with the potential for self-renewal and multi-lineage differentiation that recapitulates the phenotype of the original tumor is designated tumor stem cells, and tumor stem cell-targeting has been considered as a novel strategy for the therapy of the malignant tumors. . Long non-coding RNAs(lncRNAs)are RNA transcripts longer than 200 bp without no protein coding capacity．Compared to short ncRNAs, the functions of lncRNAs are less understood. The spatio-temporal expression profiles of some lncRNAs indicate they may have magnificent physiological and biochemical functions.Recent studies show that lncRNA MEG3 could regulate glioma development. The expression of MEG3 is markedly decreased in glioma tissues compared with adjacent normal tissues. Overexpression of MEG3 inhibites cell proliferation and promotes cell apoptosis. MEG3 also facilitated JARID2-PRC2 interactions on chromatin that is required for the differentiation of ESCs. Our previous study showed that the expression of MEG3 was also decreased significantly in glioma stem cells compared with glioma cells, suggesting that MEG3 may play a key role in regulating glioma stem cells. . In this study, we will examine the lncRNA MEG3 expression patterns in glioma stem cells. Then we will invesgate the effect of MEG3 on glioma stem cell initiation, maintenance, proliferation, differentiation and so on. Moreover, we will further focus on the probable molecular mechanism that MEG3 regulates the glioma stem cells. It will present more evidence to fully understand the effect of lncRNAs on glioma stem cells, and therefore provide theoretical and practical significance for the establishment of lncRNAs-mediated therapeutic manipulation on glioma stem cells.