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首页> 外文期刊>Molecular medicine reports >MicroRNA-379 inhibits cell proliferation and invasion in glioma via targeting metadherin and regulating PTEN/AKT pathway
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MicroRNA-379 inhibits cell proliferation and invasion in glioma via targeting metadherin and regulating PTEN/AKT pathway

机译:MicroRNA-379通过靶向Metadherin和调节PTEN / AKT途径抑制细胞增殖和胶质瘤中的侵袭

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Numerous microRNAs (miRNAs) are aberrantly expressed in glioma, and implicated in glioma occurrence and development. Therefore, the development of miRNAs as potential therapeutic targets for the treatment of patients with glioma has been proposed. miR-379 has been shown to be aberrantly expressed in the progression of malignant tumours. However, the expression, biological functions and mechanism of miR-379 in glioma are yet to be fully understood. Hence, the present study aimed to detect miR-379 expression, investigate its functional relevance and explore its associated molecular mechanism in glioma. In this study, miR-379 expression was significantly downregulated in glioma tissues and cell lines. Enforced miR-379 expression markedly suppressed the cell proliferation and invasion of glioma. Metadherin (MTDH) was identified as a direct target of miR-379 in glioma. The miR-379 expression and MTDH mRNA levels exhibited an inverse association in glioma tissues. The restoration of the MTDH expression partially rescued the inhibitory effects of miR-379 overexpression on glioma cell proliferation and invasion, and the upregulation of miR-379 inhibited the activation of phosphatase and tensin homolog (PTEN)/AKT serine/threonine kinase (AKT) signaling pathway. Overall, these findings demonstrated that miR-379 may play tumour-suppressing roles in glioma through downregulation of MTDH and regulation of the PTEN/AKT signaling pathway, suggesting that miR-379 might be a possible target for the treatment of patients with this malignancy.
机译:许多MicroRNA(miRNA)在胶质瘤中异常表达,并涉及胶质瘤发生和发育。因此,提出了MiRNA作为治疗胶质瘤患者的潜在治疗靶标的发育。 MiR-379已被证明在恶性肿瘤的进展中表达了异常表达。然而,胶质瘤中miR-379的表达,生物学功能和机制尚未得到完全理解。因此,本研究旨在检测miR-379表达,研究其功能性相关性并探讨其在胶质瘤中的相关分子机制。在本研究中,MIR-379表达在胶质瘤组织和细胞系中显着下调。强制miR-379表达明显抑制细胞增殖和胶质瘤的侵袭。 Metadherin(MTDH)被鉴定为胶质瘤MiR-379的直接靶标。 miR-379表达和MTDH mRNA水平在胶质瘤组织中表现出逆关联。 MTDH表达的恢复部分地拯救了miR-379过表达对胶质瘤细胞增殖和侵袭的抑制作用,MiR-379的上调抑制了磷酸酶和牙素同源物(Pten)/ akt丝氨酸/苏氨酸激酶(akt)的活化。信号通路。总体而言,这些研究结果证明MiR-379可以通过MTDH的下调和PTEN / AKT信号传导途径的调节在胶质瘤中发挥肿瘤抑制作用,表明miR-379可能是治疗这种恶性肿瘤患者的可能靶标。

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