Analysis of Genes Associated with Both Neural Tube Defects and Neuroectodermal Tumors

MEDICAL SCIENCE MONITOR(2022)

引用 0|浏览7
暂无评分
摘要
Background: Previous studies have demonstrated that embryo development and the occurrence of tumors are closely relat-ed, as key genes, pathways, miRNAs, and other biological mechanisms are involved in both processes. Extensive research has found that abnormal development of nerve ectodermal cells not only leads to neural tube defects (NTDs), but also neuroectodermal tumors. Material/Methods: Genes associated with both NTDs and neuroectodermal tumors were obtained from the DisGeNET database. The STRING database was used to construct the protein-protein interaction (PPI) network and the hub genes were visualized using Cytoscape. Additionally, we predicted the miRNAs targeting the identified genes. Sequencing data obtained from an NTDs mouse model and human samples were used to confirm the bioinformatics re-sults. Moreover, a dual-luciferase report assay was used to validate the targeting relationship between the miR-NA-gene pairs identified. Results: A total of 104 intersection genes of NTDs-related and neuroectodermal tumors-related genes were obtained; 20 of these genes were differentially expressed in NTDs samples and had very close interactions. Among 10 hub genes, we identified 3 important susceptibility genes differentially expressed both in RA-induced NTDs mice and human glioblastoma samples: Ncam1, Shh, and Ascl1. Among these, we found that the Ncam1 expression level was regulated by mmu-miR-30a-5p, and the Ascl1 expression level was regulated by mmu-miR-375-3p. Conclusions: In conclusion, we identified differentially expressed genes and a potential miRNA-mediated regulation mech-anism shared between NTDs and neuroectodermal tumors that may guide future studies aiming to find nov-el therapeutic targets for NTDs or neuroectodermal tumors.
更多
查看译文
关键词
ASCL1 Protein, Human, MicroRNAs, NCAM1 Protein, Neural Tube Defects, Neuroectodermal Tumors
AI 理解论文
溯源树
样例
生成溯源树,研究论文发展脉络
Chat Paper
正在生成论文摘要