Fig. 1

miR-10b is upregulated in RDEB-cSCC. a Unsupervised clustering via PCA on miRNA expression levels clearly separated RDEB-cSCC (n = 4) and HC-cSCC (n = 3) samples from RDEB-KC (n = 6) and HC-KC (n = 5). Target analysis of miR-10b, which was significantly (p ≤ 0.05) up-regulated (≥ 2-fold) in both, b HC-cSCCs and (c) RDEB-cSCCs, indicated an enrichment of pathways related to aggressive tumor phenotypes like epithelial-to-mesenchymal transition (EMT) (d). e TaqMan qPCR (n = 3 ind. repl., mean ± SEM, *p < 0.05, n.s. non-significant, unpaired t-test), as well as (f) fluorescence-based in situ hybridization (FISH) with DIG labelled miR-10b probes (green) on FFPE tissues sections of confirmed (H&E staining, top row) carcinomas also showed miR-10b dysregulation. White dashed line: tumor boundaries marked by pan-keratin staining (red). Scale bars: 100 μm (white), 500 μm (black). Sample codes (e) from left to right HC-KC: 1090KC, SKC013, SKC018; RDEB-KC: RDEB-55KC, RDEB-43KC, RDEB-29KC; RDEB-cSCC: RDEB-SCC1, RDEB-SCC2, RDEB-SCC62; HC-cSCC: SCC13, WT18SCC, A431