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首页> 外文期刊>European review for medical and pharmacological sciences. >LncRNA HANR aggravates the malignant progression of glioma via targeting miRNA-335
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LncRNA HANR aggravates the malignant progression of glioma via targeting miRNA-335

机译:LNCRNA HANR通过靶向miRNA-335加剧了胶质瘤的恶性进展

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OBJECTIVE: The aim of this study was to uncover the role of lncRNA HANR in the progression of glioma and the underlying mechanism. PATIENTS AND METHODS: HANR expression level in 36 matched glioma tissues and adjacent non-tumoral tissues was determined by qRT-PCR. The relationship between HANR expression and pathological indexes of the glioma patients was analyzed. The Kaplan-Meier method was introduced to investigate the survival of glioma patients. After the knockdown of HANR, the proliferative, migratory, and invasive changes of U251 and SHG44 cells were determined. Bioinformatics and Dual-Luciferase Reporter Gene Assay were applied to predict and verify the downstream target of HANR, respectively. Furthermore, the rescue experiments were conducted to clarify the role of HANR/miRNA-335 regulatory loop in the progression of glioma. RESULTS: HANR was significantly upregulated in glioma tissues and cell lines. Glioma patients with a high expression level of HANR presented remarkably higher rates of lymphatic metastasis and distant metastasis, as well as worse prognosis. The silence of HANR remarkably attenuated the proliferative, migratory, and invasive capacities of U251 and SHG44 cells. MiRNA-335 was the direct target of HANR and was significantly downregulated in glioma tissues. Meanwhile, the miRNA-335 level was negatively regulated by HANR. In addition, the knockdown of miRNA-335 partially reversed the regulatory effects of HANR on cellular behaviors of glioma. CONCLUSIONS: LncRNA HANR is upregulated in glioma, which is closely correlated with metastasis and poor prognosis of glioma patients. In addition, HANR aggravates the progression of glioma by negatively regulating miRNA-335.
机译:目的:本研究的目的是揭示LNCRNA HANR在胶质瘤进展中的作用和潜在机制。患者和方法:通过QRT-PCR测定36种匹配的胶质瘤组织中HANR表达水平和相邻的非肿瘤组织。分析了HANR表达与胶质瘤患者病理指标的关系。引入了Kaplan-Meier方法以研究胶质瘤患者的存活。确定HANR敲低后,确定了U251和SHG44细胞的增殖性,迁移和侵袭性变化。将生物信息学和双荧光素酶报告基因测定分别用于预测和验证HANR的下游靶标。此外,进行了救援实验,以阐明HANR / miRNA-335调节内环在胶质瘤进展中的作用。结果:HANR在胶质瘤组织和细胞系中显着上调。 HANR高表达水平的胶质瘤患者呈现出显着更高的淋巴结转移和远处转移,以及更差的预后。 HANR的沉默显着减弱了U251和SHG44细胞的增殖性,迁移和侵袭性。 miRNA-335是HANR的直接靶标,在胶质瘤组织中显着下调。同时,MiRNA-335水平由HANR负面调节。此外,miRNA-335的敲低部分逆转了HANR对胶质瘤细胞行为的调节作用。结论:LNCRNA HANR在胶质瘤上上调,与转移和胶质瘤患者的预后密切相关。此外,HANR通过对miRNA-335负面调节胶质瘤的进展加剧。

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