Figure 2.

(A) Several well-established mesenchymal marker genes (e.g., VIM and FN1) are elevated in primary HNSCC with low SOX2 expression according to TCGA (The Cancer Genome Atlas; https://cancergenome.nih.gov) (B) Inverse expression pattern between KLK6 and mesenchymal markers as well as key regulators of EMT in primary HNSCC of the TCGA cohort; (C) High expression of SOX2 contributes—among others—to the pathogenesis of HNSCC by promoting tumor cell proliferation. In advanced tumor stages, SOX2 might interfere with tumor cell plasticity and activation of mesenchymal transition by stabilization of the epithelial phenotype including stemness-like traits. KLK6 (kallikrein-related peptidase 6).