Introduction:
Angelica dahurica extract (ADE) has been demonstrated to possess functions of immune response modulation, breast injury and fibrosis amelioration, breast regeneration regulation, and suppression of breast cancer.

Material and methods:
To explore the effect of the ADE on breast cancer generation and epithelial-mesenchymal transition (EMT) in vivo, a breast cancer mouse model was established. Chinese traditional medicine ADE was administered to mice bearing breast cancer, which were randomly divided into a negative group, ADE group (two doses), and model group. The breast tissue of the mouse model was fixed and H&E staining was performed for subsequent histological observation. Immunofluorescence assay and immunohistochemical staining were performed to examine the breast cancer related proteins, SNCG and BCRP in breast tissue; Western blotting and quantitative real-time polymerase chain reaction (PCR) were performed to detect proteins and gene expression of epithelial-mesenchymal transition (EMT)-related markers, E-cadherin, N-cadherin, vimentin, transforming growth factor β (TGF-β), and SNAIL, as well as signals in the MAPK and JAK/STAT signaling pathways.

Results:
Pathological manifestation of breast tissues in ADE-treated mouse was clearly reduced in both visual inspection and H&E staining. Breast cancer specific SNCG and BCRP expression significantly decreased after ADE administration. Furthermore, increased E-cadherin and decreased N-cadherin, vimentin, SNAIL and TGF-β expression might be associated with the anti-EMT property of ADE. Both MAPK and JAK/STAT signaling pathways were observed to be inactivated after ADE treatment.

Conclusions:
Collectively, the evidence showed that ADE restrained breast cancer development in vivo through blocking the EMT process, probably by down-regulation of MAPK and JAK/STAT signaling pathways.