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Over-expression of long noncoding RNA HOTAIRM1 promotes cell proliferation and invasion in human glioblastoma by up-regulating SP1 via sponging miR-137

机译:通过冲压miR-137,通过海绵MiR-137来促进人胶质母细胞增殖和侵袭人胶质母细胞的细胞增殖和侵袭

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摘要

Glioblastoma is the most aggressive malignant brain tumor in adults. Long noncoding RNA HOTAIRM1 (HOX antisense intergenic RNA myeloid 1) has been reported to participate in the progression of various cancers. However, the role of HOTAIRM1 in glioblastoma and its underlying mechanisms are largely unknown. The relative expression levels of HOTAIRM1, miR-137 and specificity protein 1 were detected by quantitative real-time PCR or western blot. The effects of HOTAIRM1 on cell proliferation and invasion were evaluated by Cell Counting Kit-8 assay and Transwell assay, respectively. The interactions among HOTAIRM1, miR-137 and specificity protein 1 were predicted by online softwares and confirmed by luciferase reporter assay and RNA immunoprecipitation assay. The levels of HOTAIRM1 and specificity protein 1 were significantly increased while miR-137 was significantly decreased in glioblastoma tissues and cells. Knockdown of HOTAIRM1 suppressed proliferation and invasion in glioblastoma cells. Moreover, miR-137 was bound to HOTAIRM1, and specificity protein 1 was identified as a target of miR-137. The protein level of specificity protein 1 was repressed by silencing the expression of HOTAIRM1, whereas the effect was restored by inhibiting the expression of miR-137. Downregulation of HOTAIRM1 expression suppressed the proliferation and invasion of glioblastoma cells by down-regulating specificity protein 1 expression via sponging miR-137, indicating a promising strategy for glioblastoma treatment.
机译:Glioblastoma是成人中最具侵袭性的恶性脑肿瘤。据报道,长的非划分RNA Hotism1(Hox反义符号核酸髓样1)参与各种癌症的进展。然而,Hotism1在胶质母细胞瘤及其潜在机制的作用在很大程度上是未知的。通过定量实时PCR或Western印迹检测HotaIsm1,miR-137和特异性蛋白1的相对表达水平。 Hotism1对细胞增殖和侵袭的影响,分别通过细胞计数试剂盒-8测定和Transwell测定评估。通过在线软件预测HotaIrm1,miR-137和特异性蛋白1之间的相互作用,并由荧光素酶报告结果和RNA免疫沉淀测定证实。 Hotism1和特异性蛋白1的水平显着增加,而MiR-137在胶质母细胞组织和细胞中显着降低。 Hotism1的敲低抑制了胶质母细胞瘤细胞中的增殖和侵袭。此外,miR-137与Hotism1结合,并且特异性蛋白质1被鉴定为miR-137的靶标。通过沉默Hotism1的表达来抑制特异性蛋白质1的蛋白质水平,而通过抑制miR-137的表达来恢复效果。通过海绵miR-137,Hotism1表达的下调抑制了胶质母细胞瘤1的增殖和侵袭胶质母细胞瘤细胞的增殖和侵袭,表明胶质母细胞瘤治疗的有希望的策略。

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