Knockout of Calcyclin Binding Protein Impedes the Growth of Breast Cancer Cells by Regulating Cell Apoptosis and β-Catenin Signaling

Breast invasive carcinoma (BRCA) is becoming the most common malignant disease worldwide, and there is intense interest in identifying diagnostic biomarkers that can be targeted for treatment of BRCA. Recent evidence has shown that calcyclin binding protein (CacyBP) can function as either a tumor promoter or suppressor during carcinogenesis. Data in The Cancer Genome Atlas (TCGA) database show that CacyBP is overexpressed in human BRCA tissues, and high levels of CacyBP are associated with shorter overall survival. Immunohistochemical staining has shown that CacyBP levels are high in cancer tissue samples and associated with a higher likelihood of disease progression. We, therefore, conducted a knockout assay to determine the role of CacyBP in the development of BRCA. Knockout of CacyBP significantly inhibited MCF7 cell proliferation and colony formation. Apoptosis was higher in CacyBP knockout cells compared with control cells. Microarray analysis showed that the CacyBP knockout caused dysregulation of numerous genes closely related to β-catenin signaling, whereas quantitative reverse-transcription PCR and immunoblotting showed that it to be inactivated. In summary, we conclude that when overexpressed, CacyBP acts as a potential oncogene for BRCA by regulating β-catenin signaling.