# Fascin-1 Promotes Cell Metastasis through Epithelial–Mesenchymal Transition in Canine Mammary Tumor Cell Lines

## TL;DR

This study shows that Fascin-1 promotes cancer spread in dogs by increasing cell movement and changing cell structure, which could help improve treatment for canine mammary tumors.

## Contribution

The study identifies Fascin-1 as a metastasis-promoting protein in canine mammary tumors through epithelial–mesenchymal transition.

## Key findings

- Fascin-1 overexpression increases migration, adhesion, and invasion in canine mammary tumor cells.
- Fascin-1 upregulates TSPAN4 and promotes lamellipodia formation, enhancing cell movement.
- Knockdown of Fascin-1 reduces metastatic abilities in tumor cell lines.

## Abstract

Canine mammary tumors are the most common tumor in female dogs. In this study, we obtained a metastatic key protein by comparing the proteomics data of in situ tumor and metastatic cell lines from the same individual. Our results not only help to compare the difference in metastasis processes between canine mammary tumors and human breast cancer but also provide a theoretical basis for the prevention of tumor metastasis and the improvement of prognosis in dogs and humans.

Canine mammary tumors (CMTs) are the most common type of tumor in female dogs. In this study, we obtained a metastatic key protein, Fascin-1, by comparing the proteomics data of in situ tumor and metastatic cell lines from the same individual. However, the role of Fascin-1 in the CMT cell line is still unclear. Firstly, proteomics was used to analyze the differential expression of Fascin-1 between the CMT cell lines CHMm and CHMp. Then, the overexpression (CHMm-OE and CHMp-OE) and knockdown (CHMm-KD and CHMp-KD) cell lines were established by lentivirus transduction. Finally, the differentially expressed proteins (DEPs) in CHMm and CHMm-OE cells were identified through proteomics. The results showed that the CHMm cells isolated from CMT abdominal metastases exhibited minimal expression of Fascin-1. The migration, adhesion, and invasion ability of CHMm-OE and CHMp-OE cells increased, while the migration, adhesion, and invasion ability of CHMm-KD and CHMp-KD cells decreased. The overexpression of Fascin-1 can upregulate the Tetraspanin 4 (TSPAN4) protein in CHMm cells and increase the number of migrations. In conclusion, re-expressed Fascin-1 could promote cell EMT and increase lamellipodia formation, resulting in the enhancement of CHMm cell migration, adhesion, and invasion in vitro. This may be beneficial to improve female dogs’ prognosis of CMT.