To Predict the Prognosis and Immunological Characteristics of Pancreatic Cancer Based on Disulfide-Death Gene Death-Related lncRNA.

Disulfide-dependent cell death, known as disulfide death, plays a pivotal regulatory role in the onset and progression of various cancers including pancreatic cancer. Despite its significance, little attention has been given to the study of disulfide death-related long non-coding RNAs (lncRNAs) in pancreatic cancer development and progression. This study utilized data from the Cancer Genome Atlas Project (TCGA) to analyze the transcriptome of pancreatic cancer. Co-expression analysis of genes associated with disulfide death was performed and six lncRNAs closely linked to disulfide death were identified through univariate and multivariate analysis. These lncRNAs were used to develop clinical prognostic models. The prognostic value of this model was then analyzed and further investigations included pathway enrichment analysis, tumor mutation load analysis, immune cell infiltration analysis, analysis of the tumor microenvironment (TME), and drug sensitivity analysis. The developed prognostic model based on disulfide-associated lncRNAs exhibited significant prognostic value, allowing for reliable predictions of patient outcomes in pancreatic adenocarcinoma (PAAD). The analysis revealed that the six identified lncRNAs serve as independent prognostic factors, significantly correlating with patient survival and recurrence rates. Additionally, findings indicated notable differences in immune cell infiltration and drug sensitivity between high-risk and low-risk patient groups, suggesting potential therapeutic targets for enhancing treatment efficacy. Our findings revealed six disulfide death-associated lncRNAs with independent prognostic value, offering a crucial indicator for predicting the prognosis of pancreatic adenocarcinoma (PAAD) patients. Additionally, the analysis of tumor immune invasion and drug sensitivity provides a novel avenue for controlling tumor invasion and metastasis as well as reducing drug tolerance.