Canine heat shock protein 27 promotes proliferation, migration, and doxorubicin resistance in the canine cell line DTK-F

- This study provides evidence for a role of HSP27 in canine mammary tumors.
- cHSP27 overexpression promotes proliferation, migration, and increased doxorubicin resistance.
- Two mouse monoclonal antibodies against cHSP27 were effective in Western blotting.

Canine mammary tumors (CMTs) are the most common type of tumors in female dogs. Heat shock proteins are highly expressed in many cancers and are involved in tumor progression and chemoresistance in CMTs; however, the biological role of canine heat shock protein 27 (cHSP27) in CMTs has not been thoroughly characterized. This study investigated the roles of cHSP27 in cell growth, migration, anchorage, and resistance to doxorubicin (DOX) using DTK-F cells, a CMT cell line that does not express cHSP27.DTK-F cells were transfected with cHSP27 and stable overexpression was established. A mouse monoclonal antibody against cHSP27 was also produced. The biological functions of cHSP27 in DTK-F cells were then evaluated using a variety of assays. Overexpression of cHSP27 was associated with increased cell proliferation, clone formation, migration, and decreased DOX sensitivity. In conclusion, these data provide evidence that cHSP27 overexpression can promote anchorage-independent growth, migration, and increased DOX resistance in CMT cells.