RBBP4 plays a vital role in the malignant progression of triple-negative breast cancer by regulating epithelial-mesenchymal transition.

Abstract

Mounting findings have revealed the increasingly appreciated functional importance of Retinoblastoma binding protein (RBBP) family members in tumorigenesis. However, the biological function of RBBP4 in breast cancer, especially in the most malignant and aggressive subtype, i.e., triple-negative breast cancer (TNBC), remains to be elucidated. The present study was aimed at elucidating the role of RBBP4 in TNBC pathogenesis. The expression of RBBP4 in TNBC tissues and cell lines was examined and its oncogenic-related functions were verified by performing a series of in vitro and in vivo experiments. At the cellular and tissue level, a marked increase in the RBBP4 expression was observed. Functionally, RBBP4 knockdown dramatically inhibited the proliferation, invasion, and migration of TNBC cells in vitro. Further, mechanistically, RBBP4 downregulation regulated the inactivation of epithelial-mesenchymal transition (EMT) of TNBC cells. In vivo xenograft model in nude mice also validated these results. Collectively, our results showed that the inhibition of RBBP4 suppresses the malignant progression of TNBC cells by regulating EMT. Thus, RBBP4 could serve as a novel biomarker and target for TNBC diagnosis and treatment.