Integrated analysis of single‑cell and bulk RNA sequencing data to construct a risk assessment model based on plasma cell immune‑related genes for predicting patient prognosis and therapeutic response in lung adenocarcinoma.

Plasma cells serve a crucial role in the human immune system and are important in tumor progression. However, the specific role of plasma cell immune-related genes (PCIGs) in tumor progression remains unclear. Therefore, the present study aimed to establish a risk assessment model for patients with lung adenocarcinoma (LUAD) based on PCIGs. The data used in the present study were obtained from The Cancer Genome Atlas and the Gene Expression Omnibus databases. After identifying nine PCIGs, a risk assessment model was constructed and a nomogram was developed for predicting patient prognosis. To explore the molecular mechanism and clinical significance, gene set enrichment analysis (GSEA), tumor mutational burden (TMB) analysis, tumor microenvironment (TME) analysis and drug sensitivity prediction were performed. Furthermore, the accuracy of the model was validated using reverse transcription-quantitative PCR (RT-qPCR). The present study constructed a risk assessment model consisting of nine PCIGs. Kaplan-Meier survival curves indicated a worse prognosis in the high-risk subgroup (risk score ≥0.982) compared with that in the low-risk subgroup. The nomogram exhibited predictive value for survival prediction (area under the curve=0.727). GSEA enrichment analysis revealed enrichment of the focal adhesion and extracellular matrix-receptor interaction pathways in the high-risk group. Moreover, the high-risk group exhibited a higher TMB, as demonstrated by the TME analysis showing lower ESTIMATE scores. Drug sensitivity prediction facilitated potential drug selection. Subsequently, differential gene expression was validated in multiple LUAD cell lines using RT-qPCR. In conclusion, the risk assessment model based on nine PCIGs may be used to predict the prognosis and drug selection in patients with LUAD.