CCNB2, NUSAP1, GTSE1, and TK1: potential dual biomarkers for pneumonia and lung adenocarcinoma

This study aimed to identify shared molecular mechanisms and potential biomarkers linking lung adenocarcinoma (LUAD) and pneumonia, conditions associated with pulmonary inflammation and cancer progression. Transcriptomic datasets for pneumonia (GSE196399 and GSE202947) and LUAD (GSE19188 and GSE31210) were analyzed using the limma package in R. Overlapping differentially expressed genes were identified, and protein-protein interaction networks were constructed via STRING. Hub genes were screened using CytoHubba and validated through ROC, survival, and genomic analyses. Functional validation included siRNA-mediated knockdown of CCNB2 and NUSAP1 in A549 and H1975 cells, followed by RT-qPCR, Western blotting, proliferation, colony formation, and wound-healing assays. Sixty-two genes were co-dysregulated in LUAD and pneumonia. Four hub genes (CCNB2, GTSE1, TK1, NUSAP1) were significantly upregulated, showed strong diagnostic accuracy (AUC 0.75-0.90), and correlated with poor survival. Knockdown of CCNB2, NUSAP1, GTSE1, and TK1 suppressed proliferation and migration in LUAD cells. CCNB2, GTSE1, TK1, and NUSAP1 are shared molecular drivers of LUAD and pneumonia, offering diagnostic, prognostic, and therapeutic potential.

The online version contains supplementary material available at 10.1007/s10616-026-00940-w.