Biotechnological Insights into KAT2A-Mediated Epigenetic Regulation in Colorectal Cancer: A Transcriptomic and Functional Genomics Approach.

Epigenetic modifiers such as lysine acetyltransferase 2A (KAT2A) have been reported to be the key regulators of gene expression in various cancers, including colorectal cancer (CRC). The transcriptomic effect of KAT2A deficiency in CRC and its implication on cancer-related pathways remains poorly elucidated. The objective of this research was to investigate genome-wide transcriptional alterations induced by KAT2A knockout in colorectal cancer cells with an eye toward the recognition of putative molecular targets for diagnosis or therapy. KAT2A-knockout HCT116 cell high-throughput RNA sequencing data (GSE246881) were analyzed. Differentially expressed genes (DEGs) were defined by DESeq2. Functional enrichment analysis, including Gene Ontology (GO) and KEGG pathways, and protein-protein interaction (PPI) network building were performed using integrated bioinformatics tools. KAT2A knockout resulted in 626 DEGs, predominantly downregulated, and indicated a potential role of KAT2A as a transcriptional activator. Enrichment analyses revealed significant involvement of cancer-related pathways such as MAPK and mTOR. PPI network analysis revealed key hub genes such as AKT1, VEGFA, and PLEC that are involved in tumor growth and may be future biomarkers or therapeutic targets. KAT2A plays a pivotal role in oncogenic signaling pathways in CRC. The identified genes and pathways here present promising prospects for biotechnological application in cancer biomarker identification and targeted therapy, demonstrating the potential of KAT2A-centered regulatory networks in guiding CRC management strategies.