An integrated approach for the study of APOBEC3B associated genes and its impact on hypoxic and immune signaling pathways in ovarian cancer
Year: 2024
Type: article
Abstract: APOBEC3B is suspected to be an enzymatic source of mutation in a small number of human cancers; it has also been associated with bone leiomyosarcoma and human T-cell leukemia virus type 1. The key processes regulated or effected by APOBEC3B include gene expression, mRNA editing, particularly C -> U Conversion, and deoxycytidine deaminase activity. The main goal of this work was to do an organized investigation of the genes associated with APOBEC3B and their functional significance in human ovarian cancer. Datasets for this project were obtained from openly available sources including TCGA and GEO. Depending on the requirements for collecting the values, several bioinformatics approaches have been applied at various levels. Additionally, the changed genes were prepared for the examination of pathway enrichment after the differentially expressed genes had been obtained. We identified numerous significant pathways that are directly related to ovarian cancer that are altered as a result of altered gene expression patterns and mutational alterations. APOBEC3B and some of these genes are related. The cell cycle, p53 signaling, immunological signaling pathways, progesterone-mediated oocyte maturation, apoptosis, and critical metabolic pathways are among the most severely damaged processes. In terms of these pathways components (genes), we conclude that TP53, TTN, MUC16, CSMD3, USH2A, BRCA1, HMCN1, CCDC26, PCAT2, PVT1, MYC, CCAT1, PCAT1, MECOM, AHNAK, PAK1, SKAP1, DNM2, SORL1, RRM1/2, CDK2, SMC4, CCNB2, CDC20, MELK, and ATAD2 appear to be highly significant based on gene expression, mutational, CNAs, SVs, network analysis.
Source: Global Journal of Basic Science
DOI: 10.63454/jbs20000012
Authors: Nawal Helmi, Dalia Alammari
Language: English
Subfield: Reproductive Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
OpenAlex ID: W4409831133
