A novel disulfidptosis-related prognostic gene signature and experimental validation identify as a novel therapeutic target in lung adenocarcinoma.

BACKGROUNDLung adenocarcinoma (LUAD) is a prevalent form of malignancy globally. Disulfidptosis is novel programmed cell death pathway based on disulfide proteins, may have a positive impact on the development of LUAD treatment strategies.OBJECTIVETo investigate the impact of disulfidptosis-related genes (DRGs) on the prognosis of LUAD, developed a risk model to facilitate the diagnosis and prognostication of patients. We also explored (DRGs) as a new therapeutic biomarker for LUAD.METHODSWe investigated the expression patterns of DRGs in both LUAD and noncancerous tissues. To assess the prognostic value of the DRGs, we developed risk models through univariate Cox analysis and lasso regression. The expression and function of was evaluated by qRT-PCR, immunohistochemistry and experiments. The TIMER examined the association between expression and immune infiltration in LUAD.RESULTSTen differentially expressed DRGs were identified. And was identified as potential risk factors through univariate Cox regression analysis ( <  0.05). expression and riskscore were used to construct a risk model to predict overall survival in LUAD, and high-risk demonstrated a significantly higher mortality rate compared to the low-risk cohort. qRT-PCR and immunohistochemistry assays indicated was upregulated in LUAD, and the upregulation was associated with clinicopathologic features. experiments showed the knockdown of expression inhibited the proliferation in LUAD cells. The TIMER analysis demonstrated a correlation between the expression of and the infiltration of diverse immune cells. Elevated expression was associated with a reduction in memory B cell count. Additionally, the expression was associated with m6A modification genes.CONCLUSIONSOur study introduced a prognostic model based on DRGs, which could forecast the prognosis of patients with LUAD. The biomarker exhibits promise for the diagnosis and management of LUAD, given its correlation with tumor immune infiltration and m6A modification.