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Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell Proliferation and Invasion by Interacting with MiR-16

机译:长的基因间非编码RNA 00152通过与MiR-16相互作用促进神经胶质瘤细胞的增殖和侵袭

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Background/Aims Long noncoding RNAs (lncRNAs) are a novel class of protein-noncoding transcripts that are aberrantly expressed in multiple diseases including cancers. LINC00152 has been identified as an oncogene involved in many kinds of cancer; however, its expression pattern and function in human glioma remain unclear. Methods Quantitative real-time polymerase chain reaction was carried out to measure LINC00152 expression in human glioma cell lines and tissues. CCK-8 and EdU assays were performed to assess cell proliferation, and scratch assays and Transwell assays were used to assess cell migration and invasion, respectively. Luciferase reporter assays were carried out to determine the interaction between miR-16 and LINC00152. In vivo experiments were conducted to assess tumor formation. Results LINC00152 was found to be significantly upregulated in human glioma cell lines and clinical samples. Knockdown of LINC00152 suppressed glioma cell proliferation, migration, and invasion in vitro. In vivo assays in nude mice confirmed that LINC00152 knockdown inhibits tumor growth. Furthermore, mechanistic investigation showed that LINC00152 binds to miR-16 in a sequence-specific manner and suppresses its expression. miR-16 inhibition strongly attenuated LINC00152 knockdown–mediated suppressive effects on proliferation, migration, and invasion. Moreover, LINC00152 induced BMI1 expression by sponging miR-16; this effect further promoted glioma cell proliferation and invasion. Conclusion We regard LINC00152 as an oncogenic lncRNA promoting glioma cell proliferation and invasion and as a potential target for human glioma treatment.
机译:背景/目的长非编码RNA(lncRNA)是一类新型的蛋白质非编码转录本,在多种疾病(包括癌症)中异常表达。 LINC00152被鉴定为涉及多种癌症的致癌基因。然而,其在人类神经胶质瘤中的表达模式和功能仍不清楚。方法采用定量实时聚合酶链反应法检测LINC00152在人脑胶质瘤细胞系和组织中的表达。进行CCK-8和EdU测定以评估细胞增殖,并且分别使用划痕测定和Transwell测定来评估细胞迁移和侵袭。进行萤光素酶报告基因测定,以确定miR-16和LINC00152之间的相互作用。进行体内实验以评估肿瘤形成。结果发现LINC00152在人神经胶质瘤细胞系和临床样品中显着上调。敲除LINC00152可抑制神经胶质瘤细胞的体外增殖,迁移和侵袭。裸鼠体内试验证实LINC00152抑制可抑制肿瘤生长。此外,机理研究表明,LINC00152以序列特异性方式与miR-16结合并抑制其表达。 miR-16的抑制作用大大减弱了LINC00152敲低介导的对增殖,迁移和侵袭的抑制作用。此外,LINC00152通过使miR-16海绵化来诱导BMI1表达;这种作用进一步促进了胶质瘤细胞的增殖和侵袭。结论我们认为LINC00152是促进神经胶质瘤细胞增殖和侵袭的致癌lncRNA,并且是人类神经胶质瘤治疗的潜在靶标。

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