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首页> 外文期刊>Journal of Cancer >Long Intergenic Noncoding RNA 00261 Acts as a Tumor Suppressor in Non-Small Cell Lung Cancer via Regulating miR-105/FHL1 Axis
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Long Intergenic Noncoding RNA 00261 Acts as a Tumor Suppressor in Non-Small Cell Lung Cancer via Regulating miR-105/FHL1 Axis

机译:长性非依赖性非数性RNA 00261通过调节MiR-105 / FHL1轴作为非小细胞肺癌中的肿瘤抑制剂

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Purpose: Long noncoding RNAs (lncRNAs) have recently received more attention for their roles in tumor progression. LINC00261 was studied in this research to identify how it affects the progression of non-small cell lung cancer (NSCLC). Methods: Firstly, the expression of LINC00261 in NSCLC cells and paired samples of NSCLC tissue was detected by RT-qPCR. Then, the associations between LINC00261 expression level and clinicopathological characteristics were evaluated. Furthermore, functional assays of cell proliferation, colony formation and transwell, as well as western blot assay, luciferase assay and RNA immunoprecipitation (RIP) assay were conducted. Afterwards, the effects of LINC00261 expression on NSCLC formation and growing were confirmed by in vivo models. Results: As results, expression of LINC00261 was significantly down-regulated in tumor samples than that in normal samples, which was correlated with the lymphatic metastasis, tumor size, tumor stage as well as patient survival time. Knockdown of LINC00261 inhibited tumor growth and invasion ability in vitro . In addition, miR-105 was identified as a direct target of LINC00261 via mechanism experiments and its expression in tumor tissues negatively correlated to LINC00261 expression. Further experiments found that Four and expression of Half LIM domains 1 (FHL1) was negatively correlated with miR-105 but positively with LINC00261. Moreover, in vivo assays verified the overexpression of LINC00261 could suppress formation of NSCLC and regulate the expression of miR-105/FHL1 axis. Conclusions: These results indicate that LINC00261 could suppress metastasis and proliferation of NSCLC via suppressing miR-105/FHL1 axis, which may offer a new vision for interpreting the mechanism of NSCLC development.
机译:目的:长时间的NOODING RNA(LNCRNA)最近在肿瘤进展中获得了其作用的更多关注。在该研究中研究了LINC00261以确定它如何影响非小细胞肺癌的进展(NSCLC)。方法:首先,通过RT-QPCR检测NSCLC细胞中LINC00261和NSCLC组织配对样品的表达。然后,评估了LINC00261表达水平和临床病理特征之间的关联。此外,进行细胞增殖,菌落形成和转槽的功能性测定,以及蛋白质印迹测定,荧光素酶测定和RNA免疫沉淀(RIP)测定。然后,通过体内模型证实了LINC00261表达对NSCLC形成和生长的影响。结果:结果:结果:结果,LINC00261的表达在肿瘤样本中显着下调,而不是正常样品,其与淋巴结转移,肿瘤大小,肿瘤阶段以及患者存活时间相关。 LINC00261的敲低在体外抑制肿瘤生长和侵袭能力。此外,MiR-105通过机制实验鉴定为LINC00261的直接靶标及其在与LIC00261表达的肿瘤组织中的表达呈负相关。进一步的实验发现,半雷米域1(FHL1)的四种和表达与miR-105呈负相关,但与LINC00261正面相关。此外,在体内测定中验证了LINC00261的过表达可以抑制NSCLC的形成并调节miR-105 / FHL1轴的表达。结论:这些结果表明,LINC00261可以通过抑制miR-105 / FHL1轴来抑制NSCLC的转移和增殖,这可能提供一种新的视野,用于解释NSCLC发育的机制。

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