SIRT2 as a Potential Biomarker in Lung Adenocarcinoma: Implications for Immune Infiltration.

SIRT2 play important roles in cell cycle and cellular metabolism in the development of non-small cell lung cancer (NSCLC), and SIRT2 exhibits its therapeutic effect on NSCLC tumors with high expression of SIRT2. Nevertheless, the clinical relevance of SIRT2 in lung adenocarcinoma (LUAD), particularly its impact on tumor growth and prognostic implications, remains obscure. This investigation entailed a comprehensive analysis of SIRT2 mRNA and protein expression levels in diverse tumor and corresponding healthy tissues, utilizing databases such as TIMER 2.0, UALCAN, and HPA. Prognostic correlations of SIRT2 expression in LUAD patients, stratified by distinct clinicopathological characteristics, were evaluated using the KM Plotter database. Additionally, the TCGA and TIMER 2.0 databases were employed to assess the relationship between SIRT2 and immune infiltration, as well as to calculate immunity, stromal, and estimation scores, thus elucidating the role of SIRT2 in modulating tumor immunotherapy responses. Furthermore, Gene Set Enrichment Analysis (GSEA) was utilized to elucidate SIRT2's biological functions in pan-cancer cells. Our findings revealed a marked reduction in both mRNA and protein levels of SIRT2 in LUAD tumors relative to healthy tissue. Survival analysis indicated that diminished SIRT2 expression correlates with adverse prognostic outcomes in LUAD. Furthermore, SIRT2 expression demonstrated a significant association with various clinicopathologic attributes of LUAD patients, influencing survival outcomes across different clinicopathologic states. Functional enrichment analyses highlighted SIRT2's involvement in cell cycle regulation and immune response. Notably, SIRT2 exhibited a positive correlation with immune cell infiltration, including natural killer (NK) cells, macrophages, and dendritic cells (DCs). In summary, SIRT2 was a potential prognostic biomarker for LUAD and and a new immunotherapy target.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)