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首页> 外文期刊>Cancer Management and Research >ZNF671 Inhibits the Proliferation and Metastasis of NSCLC via the Wnt/β-Catenin Pathway
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ZNF671 Inhibits the Proliferation and Metastasis of NSCLC via the Wnt/β-Catenin Pathway

机译：ZnF671通过Wnt /β-catenin途径抑制NSCLC的增殖和转移

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Background: Lung cancer is the most common cancer in the world and is the main cause of cancer-related death. Revealing the potential mechanism of malignant characteristics of lung cancer is urgent for treating this disease effectively. Zinc finger protein 671 (ZNF671) is a member of the largest transcription factor family in the human genome. The role of ZNF671 in non-small-cell lung cancer (NSCLC) remains unknown. The purpose of this study was to investigate the function and mechanism of ZNF671 in NSCLC. Methods: ZNF671 expression in NSCLC cells and tissues were detected by Real-Time PCR, Western blot and TCGA databases. Then, we evaluated the prognostic value of ZNF671 expression in NSCLC using the Kaplan–Meier plotter (KM plotter) and TCGA databases. Moreover, the function of ZNF671 in the proliferation and metastasis of lung cancer was investigated by MTT assay, colony formation assay, in vivo experiment, EdU assay, wound healing assay, transwell assay, and 3D culture assay. Luciferase reporter and subcellular fractionation assays were performed to determine the underlying mechanism of ZNF671-mediated proliferation and metastasis of NSCLC. Results: ZNF671 expression was significantly reduced in both NSCLC cell lines and clinical specimens compared to that in normal controls. The survival analysis results indicated that the downregulation of ZNF671 significantly correlates with poor prognosis and predicts a shorter overall survival and post-progression survival among NSCLC patients. Ectopic overexpression of ZNF671 dramatically restrains, whereas silencing ZNF671 enhanced, cell proliferation and metastasis of NSCLC. Mechanically, gene set enrichment analysis (GSEA) showed that the expression of ZNF671 was significantly correlated with Wnt/β-catenin signaling. Simultaneously, our results confirm that the overexpression of ZNF671 inhibits cell cycle progression and metastasis by weakening the Wnt/β-catenin pathway, and then downregulating the expression of downstream target genes CyclinD1 and MMP9. Conclusion: This study found that the overexpression of ZNF671 restrains the proliferation and metastasis of lung cancer through inhibiting Wnt/β-catenin signaling pathway. Furthermore, our current results provide important insights into ZNF671 as an excellent predictive biomarker for NSCLC, thus providing a novel perspective for the treatment of NSCLC.
机译：背景：肺癌是世界上最常见的癌症，是癌症相关死亡的主要原因。揭示肺癌恶性特征的潜在机制是有效治疗这种疾病的迫切需要。锌指蛋白671（ZNF671）是人类基因组中最大的转录因子家族的成员。 ZNF671在非小细胞肺癌（NSCLC）中的作用仍然未知。本研究的目的是研究ZNF671在NSCLC中的功能和机制。方法：通过实时PCR，Western印迹和TCGA数据库检测NSCLC细胞和组织中的ZNF671表达。然后，我们使用Kaplan-Meier绘图仪（KM绘图仪）和TCGA数据库评估了NSCLC中ZNF671表达的预后值。此外，通过MTT测定，菌落形成测定，体内实验，EDU测定，伤口愈合测定，Transwell测定和3D培养测定，研究了ZnF671在肺癌增殖和转移中的功能。进行荧光素酶报告器和亚细胞分级测定以确定ZNF671介导的含有NSCLC的增殖和转移的潜在机制。结果：与正常对照相比，NSCLC细胞系和临床标本的表达显着降低了ZNF671表达。生存分析结果表明，ZNF671的下调与预后差明显相关，并预测NSCLC患者中的较短的整体存活率和进展后生存率。 ZnF671的异位过表达显着抑制，而沉默ZNF671增强，细胞增殖和NSCLC转移。机械地，基因设定富集分析（GSEA）表明ZnF671的表达与Wnt /β-catenin信号传导显着相关。同时，我们的结果证实ZnF671的过表达通过削弱Wnt /β-catenin途径，然后下调下游靶基因Cyclind1和MMP9的表达来抑制细胞周期进展和转移。结论：本研究发现，通过抑制Wnt /β-catenin信号传导途径，ZnF671的过表达抑制了肺癌的增殖和转移。此外，我们的目前的结果为ZnF671提供了重要的见解，作为NSCLC的优异预测生物标志物，从而为治疗NSCLC提供了一种新颖的视角。

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