KAT2A: a prognostic biomarker influencing proliferation and immune escape in lung adenocarcinoma

Lung adenocarcinoma (LUAD) is the most prevalent histological subtype of lung cancer, characterized by high mortality rates. KAT2A has been implicated in oncogenic processes and tumor progression. This study systematically investigated the role of KAT2A in LUAD through comprehensive analyses. Expression profiles and prognostic significance of KAT2A were evaluated using TCGA database and multiple GEO datasets. Functional enrichment analyses including GO and KEGG pathway analyses were conducted to elucidate biological mechanisms associated with KAT2A-regulated differentially expressed genes. Correlations between KAT2A expression levels and immune cell infiltration were analyzed using R software and publicly available databases. Experimental validation was performed through CCK-8 assays, colony formation assays, flow cytometry, and xenograft tumor models. Our findings demonstrated significantly elevated KAT2A expression in LUAD tissues and cells. Expression levels correlated with multiple clinicopathological parameters including TNM stage, pathological stage, sex, and tumor localization. High KAT2A expression was associated with reduced overall survival and exhibited prognostic relevance across diverse clinical subgroups. Multivariate analysis confirmed independent prognostic value of KAT2A expression in the established nomogram model. Functional annotation revealed enrichment of KAT2A-associated genes in critical biological processes and signaling pathways. Moreover, KAT2A expression exhibited correlations with mutational profiles and immune cell infiltration patterns in LUAD. Both in vitro and in vivo experiments demonstrated that KAT2A knockdown significantly suppressed tumor cell proliferation and immune evasion mechanisms, induced apoptosis, and inhibited tumor growth. These findings suggest that KAT2A may serve as a potential prognostic biomarker for LUAD, with therapeutic implications through its regulatory role in immune evasion pathways.