Zheng Ying-Juan, Liang Tian-Song, Wang Juan, Zhao Jing-Yi, Yang Dao-Ke, Liu Zhang-Suo
Department of Radiotherapy, The Tumor Hospital of the First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, P.R. China.
Department of Radiotherapy, The Tumor Hospital of the First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, P.R. China.
Mol Ther Nucleic Acids. 2019 Dec 6;18:485-495. doi: 10.1016/j.omtn.2019.07.026. Epub 2019 Aug 31.
Long non-coding RNAs (lncRNAs) have been widely highlighted due to their involvement in various types of cancers, including glioma; however, the exact mechanism and function by which they operate in regard to spinal cord glioma remain poorly understood. LOC101928963 was screened out for its differential expression in spinal cord glioma by microarray analysis. Therefore, this study was conducted to investigate the modulatory effects of LOC101928963 on spinal cord glioma by binding to phorbol-12-myristate-13-acetate-induced protein 1 (PMAIP1). The expression of LOC101928963 and LOC101928963 was characterized in spinal cord glioma tissues, and their interaction was examined by dual-luciferase reporter gene assay. Cells with LOC101928963 that exhibited elevated or suppressed levels of PMAIP1 were established to substantiate the mechanism between LOC101928963 and PMAIP1. qRT-PCR and western blot methods were subsequently applied to determine the expression of cell-proliferation- and apoptosis-related genes in response to the alterations of LOC101928963 and PMAIP1. Glioma cell proliferation and apoptosis were assessed by MTT assay and flow cytometry. Decreased cell apoptosis and PMAIP1 expression, as well as overexpressed LOC101928963, were exhibited among spinal cord glioma tissues. LOC101928963 overexpression was observed to promote cell proliferation and cell-cycle entry and inhibit the process of apoptosis. PMAIP1, a target of LOC101928963, displayed a downregulated level following the elevation of LOC101928963. The present results strongly emphasize the neutralization effect of PMAIP1 overexpression on spinal cord glioma progression induced by the overexpression of LOC101928963. The data obtained during the study highlighted the inhibitory role of LOC101928963 silencing in spinal cord glioma through the increase in PMAIP1, which suggests a potential target in the treatment of spinal cord glioma.
长链非编码RNA（lncRNAs）因其参与包括神经胶质瘤在内的多种癌症而受到广泛关注；然而，它们在脊髓神经胶质瘤中的具体作用机制和功能仍知之甚少。通过微阵列分析筛选出在脊髓神经胶质瘤中差异表达的LOC101928963。因此，本研究旨在通过与佛波醇-12-肉豆蔻酸酯-13-乙酸酯诱导蛋白1（PMAIP1）结合来研究LOC101928963对脊髓神经胶质瘤的调节作用。对脊髓神经胶质瘤组织中LOC101928963和PMAIP1的表达进行了表征，并通过双荧光素酶报告基因测定法检测了它们之间的相互作用。建立了PMAIP1水平升高或降低的LOC101928963细胞，以证实LOC101928963与PMAIP1之间的机制。随后应用qRT-PCR和蛋白质印迹法来确定细胞增殖和凋亡相关基因在LOC101928963和PMAIP1改变后的表达。通过MTT法和流式细胞术评估神经胶质瘤细胞的增殖和凋亡。在脊髓神经胶质瘤组织中观察到细胞凋亡和PMAIP1表达降低，以及LOC101928963过表达。观察到LOC101928963过表达促进细胞增殖和细胞周期进入，并抑制凋亡过程。PMAIP1是LOC101928963的一个靶点，在LOC101928963升高后其水平下调。目前的结果强烈强调了PMAIP1过表达对LOC101928963过表达诱导的脊髓神经胶质瘤进展的中和作用。研究期间获得的数据突出了LOC101928963沉默通过增加PMAIP1对脊髓神经胶质瘤的抑制作用，这表明其可能是治疗脊髓神经胶质瘤的一个潜在靶点。
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