Tranexamic acid can inhibit tongue squamous cell carcinoma invasion in vitro

Abstract

Tranexamic acid (TA) is an inhibitor of plasminogen activation commonly used in surgery. Plasmin, the end product of plasminogen activation, degrades fibrin in the thrombus, leading to thrombolysis. However, plasmin is also associated with progression of several cancers and with cancer-associated matrix metalloproteinase-9 (MMP-9) activation. As the gelatinases MMP-2 and -9 are involved in cancer progression, several antigelatinolytic drugs have been developed as potential anticancer therapeutics. We previously developed gelatinases targeting peptide CTT1 capable of inhibiting carcinoma growth. The effects of TA and CTT1 on tongue carcinoma aggressiveness were evaluated in an in vitro assay of human HSC-3 and SCC-25 cells. The cells were cultured with or without TA and CTT1 and their proMMP-9 production and activation were analysed with Western immunoblotting and gelatin zymography. Their effects on tongue carcinoma invasion were analysed in a Matrigel assay. Tranexamic acid alone and in combination with CTT1 can inhibit tongue SCC invasion in vitro, at least partially explained by its property of reducing the plasmin-mediated activation of proMMP-9. These data suggest that patients undergoing surgical therapy for large oral malignancies may cobenefit from prolonged TA therapy, because of its antithrombolytic and antitumour properties.