Fig 2: KCNAB2-related differentially expressed genes (DEGs) and functional enrichment analysis using GO and KEGG. (A) Volcano plot of DEGs. Blue and red dots indicate the significantly downregulated and upregulated DEGs. (B) Top 10 terms of KEGG analysis of upregulated DEGs. (C–E) Top 20 terms of GO analysis of DEGs, including biological process (BP), molecular function (MF), and cellular component (CC).

Fig 3: Associations between the expression of KCNAB2 and the overall survival based on LUAD patients with different clinical parameters. (A) Stage I–II, (B) N0, (C) N1–N3, (D) M0, (E) age over 65 years old, and (F) smoker over 40 years.

Fig 4: Real-time PCR results for analyzing the expression of tumor immune-related chemokines. (A) The overexpression effect of KCNAB2 in A549 cell line and H23 cell line was verified at the mRNA and protein levels. (B,C) Chemokines, including CCL2, CCL3, CCL4, CCL18, CXCL9, CXCL10, and CXCL12, were upregulated by KCNAB2 in A549 (B) and H23 cell lines (C). * p < 0.05, ** p < 0.01, *** p < 0.001.

Fig 5: Clinical significance of KCNAB2 in LUAD. Correlation between KCNAB2 expression and clinical parameters, including (A) pathological stage, (B–D) TNM stage, (E) primary therapy outcomes, (F) gender, (G) age, and (H) smoker. Primary therapy outcome: PD, progressive disease; SD, stable disease; PR, partial response; CR, complete response. * p < 0.05, *** p < 0.001.