Fig. 3: The IL-17 signaling pathway and S100A8/A9 are up-regulated in cervical cancer and HPV-related models.

A KEGG enrichment for genes up- and down-regulated in HPV-KI/HaCaT cells. B GSEA analysis for IL-17 signaling pathway in HPV-KI and HaCaT cells. C Heatmap displaying up- and down-regulated genes of the IL-17 signaling pathway in HPV-KI and HaCaT cells. D Comparison of IL-17 signaling pathway gene scores between CSCE and normal control in TCGA and GTEx database. E Kaplan–Meier survival analysis of CESC patients with high and low IL-17 gene scores. F GSEA analysis of the IL-17 signaling pathway in RNA-seq data from swollen ears of K14-HPV mice compared to normal FVB controls. Venn diagram illustrating the number (G) and STRING network visualization of 31 up-regulated genes (H) among HPV-KI/HaCaT cells, K14-HPV mice/FVB, and CSEC/normal control. I The TCGA database was utilized to assess the expression levels of S100A8 and S100A9 in different cancers and their corresponding normal tissues, with “S100A8(T)”, “S100A8(N)”, “S100A9(T)”, and “S100A9(N)” representing the respective expression levels in tumor and normal tissues. J Immunohistochemistry demonstrating different expression levels of S100A8/A9 in CC samples. K S100A8/A9 protein levels in HPV-KI/HaCaT cells. L Western blot analysis of ERK1/2, IκBα, phosphorylated ERK1/2 and phosphorylated IκBα protein levels in HPV-KI/HaCaT cells, with GAPDH serving as control. The data shown represent mean ± SD (Student’s t-test). P value is denoted as *P < 0.05, **P < 0.01, and ***P < 0.001, ****P < 0.0001, “ns” represents “not significant”.