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

in Environmental toxicology by Chao Zhao, Yuduo Guo, Yujia Chen, Guanjie Shang, Dixiang Song, Jun Wang, Jingjing Yang, Hongwei Zhang

TLDR

  • This study looked at a protein called ZNF207 in brain tumors called gliomas. They found that ZNF207 is more likely to be found in gliomas than in normal brain tissue. They also found that ZNF207 is associated with bad outcomes for glioma patients. They then used a special technique to silence ZNF207 in glioma cells and found that it slowed down the growth of the cells and made them more likely to die. They also found that ZNF207 is related to a process called EMT, which is important for the growth and spread of gliomas. Overall, this study suggests that ZNF207 could be a potential biomarker and therapeutic target for glioma prevention.

Abstract

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. 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. 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. ZNF207 may identify as a prospective biomarker and therapeutic candidate for glioma prevention, providing valuable insights into understanding glioma pathogenesis and treatment strategies.

Overview

  • The study aims to elucidate the role and significance of ZNF207 in glioma using online databases, bioinformatics methodologies, and in vitro assays. The hypothesis being tested is that ZNF207 plays a crucial role in gliomagenesis and has prognostic value for glioma patients. The study utilizes immunohistochemistry and RT-PCR techniques to validate the expression level of ZNF207 in glioma samples and explores its biological effects on glioma cells through in vitro assays. The primary objective of the study is to identify ZNF207 as a potential biomarker and therapeutic candidate for glioma prevention and to provide insights into understanding glioma pathogenesis and treatment strategies.

Comparative Analysis & Findings

  • The study compares the expression levels of ZNF207 in gliomas and normal brain tissue using online databases and in vitro assays. The 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. 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.

Implications and Future Directions

  • The study's findings suggest that ZNF207 may identify as a prospective biomarker and therapeutic candidate for glioma prevention. The study provides valuable insights into understanding glioma pathogenesis and treatment strategies. However, the study has limitations, such as the small sample size and the need for further validation of the results in larger studies. Future research directions could include the development of targeted therapies against ZNF207, the exploration of the role of ZNF207 in other types of brain tumors, and the investigation of the underlying molecular mechanisms of ZNF207's involvement in gliomagenesis.
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