همایش ملی بیوانفورماتیک ایران

صفحه اصلی / 4th international edition and 13th Iranian Conference on Bioinformatics

Tissue-Specific Gene Co-Expression Analysis in Pediatric Ependymomas Across Different Anatomical Regions

نویسندگان :

Zahra Eghbali¹ Mohammad Reza Zabihi² Pedram Jahangiri³ Zahra Salehi⁴

1- Hematology, Oncology and Stem Cell Transplantation Research Center, Research Institute for Oncology, Hematology and Cell Therapy, Tehran University of Medical Sciences, Tehran, Iran 2- Laboratory of Complex Biological Systems and Bioinformatics (CBB), Department of Bioinformatics, Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran 3- Hematology, Oncology and Stem Cell Transplantation Research Center, Research Institute for Oncology, Hematology and Cell Therapy, Tehran University of Medical Sciences, Tehran, Iran 4- Hematology, Oncology and Stem Cell Transplantation Research Center, Research Institute for Oncology, Hematology and Cell Therapy, Tehran University of Medical Sciences, Tehran, Iran

کلمات کلیدی :

Pediatric ependymoma،WGCNA،gene co-expression modules،hub genes،molecular heterogeneity

چکیده :

Ependymomas are central nervous system tumors that arise from ependymal cells lining the ventricles of the brain and the central canal of the spinal cord. These tumors predominantly affect pediatric populations and exhibit significant heterogeneity in location, histological features, and genetic characteristics. This study aimed to identify tissue-specific gene co-expression modules in pediatric ependymomas located in the posterior fossa, spinal cord, and cerebrum using Weighted Gene Co-Expression Network Analysis (WGCNA). By exploring these modules, we sought to uncover the molecular mechanisms underlying tumor development and heterogeneity across anatomical regions. Gene expression profiles were retrieved from the Gene Expression Omnibus (GEO) database, specifically focusing on dataset GSE27279 related to pediatric ependymomas. Following rigorous normalization and quality control procedures, WGCNA was employed to construct gene co-expression networks, enabling the identification of gene modules associated with specific tissue types (posterior fossa, spinal cord, and cerebrum). Hub genes within significant modules were identified based on intramodular connectivity, and functional enrichment analyses (GO and KEGG pathways) were conducted to elucidate their biological roles. The analysis revealed 31 modules in the supratentorial region, 54 modules in the posterior fossa, and 15 modules in the spinal cord. Among these, the blue and red gene modules exhibited significant correlation with the posterior fossa region while showing a strong negative correlation with the supratentorial and spinal cord regions. Conversely, the yellow, turquoise, and brown modules displayed significant correlation with the supratentorial region. Notably, while the yellow and turquoise modules were also significant in the posterior fossa, they demonstrated negative correlation with this region. Hub genes were identified for each module, showcasing their critical roles in tumorigenesis and tissue-specific processes. For example, in the blue module, MYO15A emerged as a key hub gene, potentially linked to cellular structural dynamics. In the brown module, MDH1B suggested a role in metabolic pathways within the tumor microenvironment. The green module's hub gene, DTL, pointed to its involvement in DNA repair and replication processes crucial for tumor proliferation. These findings highlight the molecular complexity and functional significance of tissue-specific gene networks in pediatric ependymomas. These results provide valuable insights into the tissue-specific molecular landscapes of pediatric ependymomas, highlighting key gene modules and pathways that may drive tumorigenesis and regional heterogeneity. This work lays the groundwork for future studies aimed at understanding the molecular underpinnings of ependymomas and developing targeted therapeutic strategies.

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ثمین همایش، سامانه مدیریت کنفرانس ها و جشنواره ها - نگارش 40.4.1