Tenascin-C promotes bladder cancer progression, depends on syndecan-4 and involves NF-κB signaling activation

Bladder cancer (BCa) is an unfortunately critical genitourinary tract disease with an uncertain pathology. Increasing evidence indicates that the tumor microenvironment is decisive with respect to cancer progression, and that this is driven by tumor cell interactions with stromal components. Tenascin-C (TN-C) is an important extracellular matrix (ECM) component and TN-C has been reported to be involved in other cancers, i.e. breast cancer. Expression of TN-C in BCa tissue is reported to positively correlate to BCa pathologic grade, yet the presence of urine TN-C is regarded as an independent risk factor for BCa. Thus, we assessed the value of TN-C in BCa tissues and noted that it also was increased according to tumor grade and was an independent risk factor for BCa. In fact, TN-C contributes to BCa cell migration, invasion and proliferation and this is dependent on syndecan-4 and involves NF-κB signaling activation. How syndecan-4 is linked to activation of NF-κB signaling is unclear. Our data provide a foundation for future investigations into TN-C’s contribution to BCa progression.