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Long Noncoding RNA WT1-AS Inhibit Cell Malignancy via miR-494-3p in Glioma.
Technology in Cancer Research & Treatment ( IF 2.8 ) Pub Date : 2020-05-18 , DOI: 10.1177/1533033820919759
Guangting Qiu 1 , Wenjie Tong 2 , Chenghao Jiang 1 , Qingsong Xie 1 , Jingfang Zou 1 , Cong Luo 1 , Jianwei Zhao 1 , Lu Zhang 1 , Jiang Zhao 1
Affiliation  

Primary brain tumors are a rare occurrence in comparison to other malignancies, the most predominant form being glioma. Commonly, exposure to ionizing radiations and inheritance of associated conditions such a neurofibromatosis and tuberous sclerosis are the most common causes of development of glioma. However, understanding of the molecular mechanisms that drive glioma development is limited. We explore the role of aberration of microRNA namely miR-494-3p through long noncoding RNA WT1-AS in the development of gliomas. In this study, we found that, levels of WT1-AS were significantly reduced in glioma tissues and cell lines. The miR-494-3p levels were negatively correlated with WT1-AS levels. The cellular proliferation and invasiveness decreased in WT1-AS transfected cell lines. Further the half maximal inhibitory concentration (IC50) of chemotherapeutic agent temozolomide was significantly reduced in the presence of WT1-AS. The cotransfection of WT1-AS and miR-494-3p reduced activation of phospho-AKT (p-AKT). Expression of miR-494-3p is modulated by binding to long noncoding RNA WT1-AS. Deregulation of WT1-AS leads to aberrant expression of miR-494-3p leading to hyperactivation of AKT. This malformation may result in altering protective immune responses in malignancies. Targeting of WT1-AS, miR-494-3p, and AKT may be novel therapeutic options in treatment of glioma.

中文翻译:

长非编码RNA WT1-AS通过神经胶质瘤中的miR-494-3p抑制细胞恶性肿瘤。

与其他恶性肿瘤相比,原发性脑部肿瘤很少见,其中最主要的形式是神经胶质瘤。通常,暴露于电离辐射和相关病症的遗传(例如神经纤维瘤病和结节性硬化症)是神经胶质瘤发展的最常见原因。但是,对驱动神经胶质瘤发展的分子机制的了解是有限的。我们探索通过长的非编码RNA WT1-AS的微小RNA即miR-494-3p的异常在神经胶质瘤的发展中的作用。在这项研究中,我们发现神经胶质瘤组织和细胞系中WT1-AS的水平显着降低。miR-494-3p水平与WT1-AS水平呈负相关。在WT1-AS转染的细胞系中,细胞增殖和侵袭力降低。此外,在存在WT1-AS的情况下,化疗药物替莫唑胺的半数最大抑制浓度(IC50)显着降低。WT1-AS和miR-494-3p的共转染可降低磷酸化AKT(p-AKT)的活化。通过与长的非编码RNA WT1-AS结合来调节miR-494-3p的表达。WT1-AS的失调导致miR-494-3p异常表达,从而导致AKT过度活化。这种畸形可能导致恶性肿瘤中保护性免疫反应的改变。靶向WT1-AS,miR-494-3p和AKT可能是治疗神经胶质瘤的新型治疗选择。WT1-AS的失调导致miR-494-3p异常表达,从而导致AKT过度活化。这种畸形可能导致恶性肿瘤中保护性免疫反应的改变。靶向WT1-AS,miR-494-3p和AKT可能是治疗神经胶质瘤的新型治疗选择。WT1-AS的失调导致miR-494-3p异常表达,从而导致AKT过度活化。这种畸形可能导致恶性肿瘤中保护性免疫反应的改变。靶向WT1-AS,miR-494-3p和AKT可能是治疗神经胶质瘤的新型治疗选择。
更新日期:2020-05-18
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