Abstract

Disulfidptosis is a new cell death model caused by accumulating intracellular disulfides bonding to actin cytoskeleton proteins. This study aimed to investigate the expression and prognostic value of disulfidptosis-related genes (DRGs) in lung adenocarcinoma (LUAD). The data of expression profiles and scRNA-seq were collected from TCGA and GEO databases. The different expressions of DRGs between normal and LUAD tissues were compared. The LASSO analysis and multivariate Cox regression analysis were utilized to develop a DRGs model for the prognosis evaluation in LUAD. The model's predictive accuracy was evaluated with the area under the receiver operating characteristic curve (AUC) and C-index. Survival analysis, univariate and multivariate Cox regression analysis were used to assessing the predictive value of the DRGs model. ScRNA-seq data were analyzed with "Seurat" and "Monocle 2" packages. There were significant differences in 22 DRGs between normal and tumor tissues. A model with five DRGs (ACTB, FLNB, NCKAP1, SLC3A2, SLC7A11) was constructed. The AUC and C-index of the model were significantly higher than that based on clinical parameters. Survival analysis, univariate and multivariate Cox regression analysis demonstrated risk score was an independent prognostic predictor. In the scRNA-seq study, we identified 14 clusters and 11 cell types. Clusters 2, 8, and 13 were annotated into Epithelial cells. SLC7A11 and SLC3A2, NCKAP1 and FLNB, ACTB expressed most abundantly in Epithelial cells, Endothelial cells, Naive CD4 T, respectively. We explored the expression of DRGs in LUAD and constructed a predictive DRGs model, which was stable and reliable for predicting LUAD prognosis.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.