Zinc finger Protein207 orchestrates glioma migration through regulation of epithelial‐mesenchymal transition

胶质瘤 生物 癌变 癌症研究 锌指 免疫组织化学 图谱 免疫系统 基因沉默 转录因子 免疫学 癌症 基因 蛋白质表达 遗传学
作者
Chao Zhao,Yuduo Guo,Yujia Chen,Guanjie Shang,Dixiang Song,Jun Wang,Jingjing Yang,Hongwei Zhang
出处
期刊:Environmental Toxicology [Wiley]
被引量:1
标识
DOI:10.1002/tox.24271
摘要

Abstract Background Glioma represents the predominant primary malignant brain tumor. For several years, molecular profiling has been instrumental in the management and therapeutic stratification of glioma, providing a deeper understanding of its biological complexity. Accumulating evidence unveils the putative involvement of zinc finger proteins (ZNFs) in cancer. This study aimed to elucidate the role and significance of ZNF207 in glioma. Methods Utilizing online data such as The Cancer Genome Atlas (TCGA), the Chinese Glioma Genome Atlas (CGGA), the Genotype‐Tissue Expression (GTEx) project, the Clinical Proteomic Tumor Analysis Consortium (CPTAC), and the Human Protein Atlas (HPA) databases, in conjunction with bioinformatics methodologies including GO, KEGG, GSEA, CIBERSORT immune cell infiltration estimation, and protein–protein interaction (PPI) analysis, enabled a comprehensive exploration of ZNF207's involvement in gliomagenesis. Immunohistochemistry and RT‐PCR techniques were employed to validate the expression level of ZNF207 in glioma samples. Subsequently, the biological effects of ZNF207 on glioma cells were explored through in vitro assays. Results Our results demonstrate elevated expression of ZNF207 in gliomas, correlating with unfavorable patient outcomes. Stratification analyses were used to delineate the prognostic efficacy of ZNF207 in glioma with different clinicopathological characteristics. Immunocorrelation analysis revealed a significant association between ZNF207 expression and the infiltration levels of T helper cells, macrophages, and natural killer (NK) cells. Utilizing ZNF207 expression and clinical features, we constructed an OS prediction model and displayed well discrimination with a C‐index of 0.861. Moreover, the strategic silencing of ZNF207 attenuated glioma cell advancement, evidenced by diminished cellular proliferation, weakened cell tumorigenesis, augmented apoptotic activity, and curtailed migratory capacity alongside the inhibition of the epithelial‐mesenchymal transition (EMT) pathway. Conclusions ZNF207 may identify as a prospective biomarker and therapeutic candidate for glioma prevention, providing valuable insights into understanding glioma pathogenesis and treatment strategies.
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