Wild-type p53 suppresses formin-binding protein-17 (FBP17) to reduce invasion

Abstract

Abstract Invading tumor cells develop membrane protruding structures called invadopodia to invade and metastasize. Previously, we have reported the role of formin-binding protein-17 (FBP17) in extracellular matrix degradation and invadopodia formation in breast cancer cells. Here, we report a novel axis between tumor-suppressor p53 and FBP17. We observed that cell lines with mutant p53 express FBP17 to a higher level. The expression of FBP17 was reduced upon stabilizing wild-type p53. Furthermore, the immunohistochemistry analysis of breast cancer tissue microarrays demonstrated the correlation between the accumulation of p53 and enhanced FBP17 staining in invasive ductal carcinomas. The double knockdown of p53 and FBP17 showed the contribution of FBP17 in the invasion of cancer cells where p53 lost the regulatory control over FBP17. Taken together, these studies indicate that FBP17 may be a marker to understand the invasion propensity of breast cancer.