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. 2019 Nov 14;20(22):5707. doi: 10.3390/ijms20225707

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Collagen VII (COL7) deficiency in recessive dystrophic epidermolysis bullosa (RDEB) skin and extracutaneous tissues favors squamous cell carcinoma (SCC) development. The figure summarizes literature findings on relevant pro-tumorigenic processes triggered by COL7 loss in RDEB keratinocytes, fibroblasts and lymphoid organs [42,44,49,52,57,58,59,61,62,63,64,67,84]. Red up arrows indicate increase/up-regulation, green down arrows indicate decrease/down-regulation. Abbreviations: ECM, extracellular matrix; ELMO2, engulfment and cell motility 2; FAK, focal adhesion kinase; ITGA6, integrin subunit alpha 6; LM332, laminin-332; LOX, lysyl oxidase; LTBP1, latent-transforming growth factor beta-binding protein 1; MMP2, metalloproteinase 2; OATP1B3, organic anion transporting polypeptide 1B3; PAR3, partitioning defective 3; PI3K, phosphoinositide 3-kinase; PLC-β4, phospholipase C-β4; RDEB, recessive dystrophic epidermolysis bullosa cutaneous; SCC, squamous cell carcinoma; SLCO1B3, solute carrier organic anion transporter family member 1B3; RDEB-SCC, RDEB-related SCC; TNC, tenascin-C; TβR1, transforming growth factor β receptor 1; TGF-β1, transforming growth factor-β1; TGM2, transglutaminase 2, VEGF, vascular endothelial growth factor.