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首页> 外文期刊>OncoTargets and therapy >LncRNA DLX6-AS1 promotes the proliferation, invasion, and migration of non-small cell lung cancer cells by targeting the miR-27b-3p/GSPT1 axis
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LncRNA DLX6-AS1 promotes the proliferation, invasion, and migration of non-small cell lung cancer cells by targeting the miR-27b-3p/GSPT1 axis

机译:LncRNA DLX6-AS1通过靶向miR-27b-3p / GSPT1轴促进非小细胞肺癌细胞的增殖,侵袭和迁移

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Background: Non-small cell lung cancer (NSCLC) has a significant impact on human health. The aim of this study was to explore the role of long non-coding RNA DLX6-AS1 in the proliferation, migration, and invasion of NSCLC cells. Methods: The expression of DLX6-AS1 in NSCLC tumor tissues and cell lines was examined by qRT-PCR. The effects of DLX6-AS1 knockdown on cell proliferation, migration, and invasion were assessed by Cell Counting Kit-8, wound healing, and transwell assays, respectively. Bioinformatics analyses, luciferase reporter assays, and RNA pull-down assays were employed to examine the mechanism by which DLX6-AS1 exerted its oncogenesis effects in NSCLC. The anti-tumor effect of silencing DLX6-AS1 in vivo was also evaluated. Results: DLX6-AS1 was over-expressed in NSCLC tumor tissues and cell lines and its level of expression was found to be associated with tumor size and advanced clinical stage in patients with NSCLC. Downregulation of DLX6-AS1 inhibited cell proliferation, cell clone formation, migration, and invasion of NSCLC cells. DLX6-AS1 was found to interact with miR-27b-3p / GSPT1. DLX6-AS1 expression was negatively correlated with miR-27b-3p expression, but positively correlated with GSPT1 expression in NSCLC samples. DLX6-AS1 knockdown also effectively suppressed tumor growth in an in vivo xenograft model. Conclusion: DLX6-AS1 regulated NSCLC progression by targeting the miR-27b-3p / GSPT1 axis, which may provide novel insights for NSCLC prognosis and therapy.
机译:背景:非小细胞肺癌(NSCLC)对人类健康有重大影响。这项研究的目的是探索长非编码RNA DLX6-AS1在NSCLC细胞的增殖,迁移和侵袭中的作用。方法:qRT-PCR检测DLX6-AS1在NSCLC肿瘤组织和细胞株中的表达。分别通过Cell Counting Kit-8,伤口愈合和transwell分析评估了DLX6-AS1敲低对细胞增殖,迁移和侵袭的影响。使用生物信息学分析,萤光素酶报告基因测定和RNA下拉测定来检验DLX6-AS1在NSCLC中发挥其致癌作用的机制。还评估了沉默DLX6-AS1体内的抗肿瘤作用。结果:DLX6-AS1在NSCLC肿瘤组织和细胞系中过表达,发现其表达水平与NSCLC患者的肿瘤大小和临床分期有关。 DLX6-AS1的下调抑制了NSCLC细胞的增殖,细胞克隆形成,迁移和侵袭。发现DLX6-AS1与miR-27b-3p / GSPT1相互作用。 DLX6-AS1表达与miR-27b-3p表达呈负相关,但与NSCLC样本中GSPT1表达呈正相关。 DLX6-AS1组合在体内异种移植模型中也能有效抑制肿瘤的生长。结论:DLX6-AS1通过靶向miR-27b-3p / GSPT1轴调控NSCLC的进展,这可能为NSCLC的预后和治疗提供新的见解。

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