Fbxo45 promotes cell viability, invasion and sunitinib resistance of clear cell renal cell carcinoma by targeting Erbin.

The mechanisms underlying the development and progression of clear cell renal cell carcinoma (ccRCC) and its sunitinib resistance are elusive. Fbxo45 is a member of the F-box protein family that has been demonstrated to participate in tumorigenesis. However, the role of Fbxo45 in ccRCC progression has not been characterized. This study aims to investigate the biological functions and molecular mechanism of Fbxo45 in ccRCC progression. We found that Fbxo45 knockdown inhibited the viability and motility of ccRCC cells, while Fbxo45 overexpression resulted in the opposite phenotype. Ectopic expression of Fbxo45 promoted tumor growth in mice. Fbxo45 expression was negatively correlated with Erbin expression, which has been reported to mediate anti-tumor activities in ccRCC. Furthermore, Fbxo45 facilitated ccRCC cell viability and motility by inhibiting Erbin. Notably, Fbxo45 upregulation reduced sunitinib sensitivity in ccRCC cells. Our results suggest that Fbxo45 could be a potential target for ccRCC treatment and sunitinib resistance.