ZNF671 Inhibits the Proliferation and Metastasis of NSCLC via the Wnt/β-Catenin Pathway.

摘要: Background Lung cancer is the most common in world and main cause of cancer-related death. Revealing potential mechanism malignant characteristics lung urgent for treating this disease effectively. Zinc finger protein 671 (ZNF671) a member largest transcription factor family human genome. The role ZNF671 non-small-cell (NSCLC) remains unknown. purpose study was to investigate function NSCLC. Methods expression NSCLC cells tissues were detected by Real-Time PCR, Western blot TCGA databases. Then, we evaluated prognostic value using Kaplan-Meier plotter (KM plotter) Moreover, proliferation metastasis investigated MTT assay, colony formation vivo experiment, EdU wound healing transwell 3D culture assay. Luciferase reporter subcellular fractionation assays performed determine underlying ZNF671-mediated Results significantly reduced both cell lines clinical specimens compared that normal controls. survival analysis results indicated downregulation correlates with poor prognosis predicts shorter overall post-progression among patients. Ectopic overexpression dramatically restrains, whereas silencing enhanced, Mechanically, gene set enrichment (GSEA) showed correlated Wnt/β-catenin signaling. Simultaneously, our confirm inhibits cycle progression weakening pathway, then downregulating downstream target genes CyclinD1 MMP9. Conclusion This found restrains through inhibiting signaling pathway. Furthermore, current provide important insights into as an excellent predictive biomarker NSCLC, thus providing novel perspective treatment