Abstract
BACKGROUND: Factor Xa (FXa) plays a role in promoting cancer growth and metastasis via protease-activated receptors. The main aim of this study was to investigate the effect of FXa inhibition, which is known to play a crucial role in cancer metabolism in hypoxia, on the behaviour of colorectal cancer cell lines HCT116 and HT29 using FXa inhibitor-rivaroxaban. METHODS: The studies were conducted under both normoxic and hypoxic conditions. The immunofluorescence method was used to assess the expression of key elements in tumor metabolism, including HIF1 alpha, LDHA, and GLUT1, following the administration of Rivaroxaban, which does not affect cell viability. RESULTS: Hypoxia resulted in increased expression of HIF1 alpha and LDHA. However, it was observed that the expression levels decreased in the rivaroxaban-treated group. It is noteworthy that no statistically significant difference was observed in GLUT1 expression. Moreover, the analysis of E-cadherin and N-cadherin expression levels revealed that Rivaroxaban significantly impacted migration under hypoxic comparison to the control group. These findings were further corroborated by the statistical results of the wound patency in the wound healing experiment. The results reveal that the inhibition of FXa with Rivaroxaban may represent a novel target for the treatment of tumor hypoxia. CONCLUSIONS: The findings of this study suggest that Rivaroxaban has the potential to be both an effective anticoagulant and an anticancer agent against CRC under both hypoxic and normoxic conditions. This paper puts forward an alternative utilization method for Rivaroxaban.