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Long noncoding RNA LINC00515 promotes cell proliferation and inhibits apoptosis by sponging miR-16 and activating PRMT5 expression in human glioma

机译:长非编码RNA LINC00515通过使miR-16海绵化并激活人胶质瘤中的PRMT5表达来促进细胞增殖并抑制细胞凋亡

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Introduction: In recent years, an increasing amount of literature has demonstrated the functional role of long non-coding RNA (lncRNA) in human diseases. LINC00515 is a newly defined lncRNA and is reported to act as an oncogene in multiple myeloma. However, the function of LINC00515 in glioma is still uncertain. Materials and methods: We examined the expression levels of LINC00515 in human glioma tissues and cell lines using real-time PCR analysis. In addition, we confirmed the distribution of LINC00515 in glioma cells and suppressed LINC00515 expression with siRNAs. CCK-8, colony formation assay and apoptosis analysis were used to study the function of LINC00515 in glioma progression. Then, we used bioinformatics prediction and subsequent experiments to reveal the underlying molecular mechanism. Results: We found that LINC00515 was up-regulated in glioma tissues and cell lines. LINC00515 was mainly located in the cytoplasm in glioma cells. Knockdown of LINC00515 led to decreased proliferation and increased apoptosis of glioma cells. Mechanistically, our data indicated that there was a LINC00515/miR-16/PRMT5 regulatory axis in glioma. LINC00515 could activate PRMT5 expression and promote glioma progression by acting as a sponge of miR-16. Conclusion: LINC00515 expression is elevated in human glioma and promotes growth and inhibits apoptosis of glioma cells. The regulatory cascade LINC00515/miR-16/PRMT5 plays a critical role in glioma progression.
机译:简介:近年来,越来越多的文献证明了长非编码RNA(lncRNA)在人类疾病中的功能。 LINC00515是新定义的lncRNA,据报道在多发性骨髓瘤中起癌基因的作用。但是,LINC00515在神经胶质瘤中的功能仍不确定。材料和方法:我们使用实时PCR分析检测了LINC00515在人脑胶质瘤组织和细胞系中的表达水平。此外,我们证实了LINC00515在神经胶质瘤细胞中的分布,并通过siRNA抑制了LINC00515的表达。使用CCK-8,集落形成试验和凋亡分析研究LINC00515在神经胶质瘤进展中的功能。然后,我们使用生物信息学预测和后续实验来揭示潜在的分子机制。结果:我们发现LINC00515在神经胶质瘤组织和细胞系中表达上调。 LINC00515主要位于神经胶质瘤细胞的细胞质中。敲低LINC00515导致神经胶质瘤细胞增殖减少和凋亡增加。从机制上讲,我们的数据表明神经胶质瘤中存在一个LINC00515 / miR-16 / PRMT5调控轴。 LINC00515可以通过充当miR-16的海绵来激活PRMT5表达并促进神经胶质瘤的进展。结论:LINC00515在人脑胶质瘤中表达升高,促进神经胶质瘤细胞的生长并抑制其凋亡。调节级联LINC00515 / miR-16 / PRMT5在神经胶质瘤进展中起关键作用。

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