FZD2 promotes TGF-?-induced epithelial-to-mesenchymal transition in breast cancer via activating notch signaling pathway

Abstract Background Breast cancer (BC) is one of the commonest female cancers, which characterized with high incidence. Although treatments have been improved, prognosis BC patients in advanced stages remains unsatisfactory. Thus, exploration molecular mechanisms underneath progression necessary to find novel therapeutic methods. Frizzled class receptor 2 (FZD2) belongs family, has proven promote cell growth and invasion various human cancers. The purpose our current study was detect functions FZD2 explore its underlying mechanism. Methods level measured tissues by quantitative real-time polymerase chain reaction (qRT-PCR), western blot, immunohistochemistry (IHC), respectively. Cell Counting Kit-8 (CCK-8), colony formation assay, transwell assays, wound healing assay flow cytometry analyses were separately conducted viability, invasion, migration, apoptosis cycle distribution. levels Epithelial-mesenchymal transition (EMT) biomarkers examined using Immunofluorescence assay. Xenograft tumorigenicity performed assess effect on tumor vivo. Results mRNA protein expression abundant tissues. Moreover, had significant correlation poor patients. In vitro functional assays revealed that silencing suppressive effects growth, migration invasion. Animal further demonstrated inhibited vivo . addition, induced EMT process cells a transforming factor (TGF)-?1-dependent manner. Mechanistically, knockdown led inactivation Notch signaling pathway. Conclusion facilitates promotes TGF-?1-inudced through activating