Carcinoma invasion is a complex process regulated by genetic and epigenetic factors as well. A relevant supportive condition for cancer cell migration is the reorganization of the extracellular matrix (ECM), which is realized in an orchestrated multicellular manner including carcinoma cells and stromal fibroblasts. An important key player in the process of ECM reorganization is Tenascin-C (Tn-C). The molecule occurs as different isoforms generated by alternative splicing and de novo glycosylation. Large variants of Tn-C are abundantly re-expressed in the invasive front of many carcinoma types. A special role for initiating migration and accompanied epithelial to mesenchymal transition has been suggested. Here, we review the current knowledge concerning the tumor biological importance of Tn-C, the synthesis and alternative splicing during the invasive process in general, and give an overview on the impact of Tn-C in urothelial carcinoma of the urinary bladder (UBC) and oral squamous cell carcinoma (OSCC).
Keywords: 3D, 3 dimensional; BM, basement membane; CAF, cancer associated fibroblast; ECM reorganization; ECM, extracellular matrix; EMT, epithelial – mesenchymal transition; FGF2, fibroblast growth factor 2; FNIII, fibronectin type III like repeats; Fn, fibronectin; Ln, laminin; Lnγ2, laminin gamma 2 chain; MMP, matrix metalloproteinase; OSCC, oral squamous cell carcinoma; PDGF, platelet derived growth factor; RNA, ribonucleic acid; TGFβ1, transforming growth factor beta 1; TPA, tetradecanoylphorbol acetate; Tn-C, tenascin-C; UBC, urothelial carcinoma of the urinary bladder; alternative splicing; carcinoma invasion; hnRNPs, heterogeneous nuclear ribonucleoproteins; mRNA, messenger RNA; oncFn, oncofetal fibronectin; oncTn-C, oncofetal tenascin-C; oral squamous cell carcinoma; tenascin-C; urothelial carcinoma of the urinary bladder.