PI3K over-expression drives canine mammary tumor progression.

Canine mammary tumor (CMT) represents the most frequently diagnosed neoplasm in intact female dogs and exhibits a high malignant rate. The PI3K/AKT pathway critically drives tumor progression, and serves as a target for multiple anti-tumor drugs. In this study, two CMT cell lines (CHMp and CIPm) were employed to assess the impact of lentivirus-mediated PI3K over-expression. Functional assays were performed to evaluate proliferation, migration, and invasion capacities, as well as the expression levels of associated proteins. As a result, PI3K over-expressing cells exhibited a significantly increase in proliferation, migration, and invasion compared to cells in negative control (NC) group. Additionally, western blot analyses revealed that PI3K over-expression evoked concordant alterations in apoptosis-related proteins, including elevated phospho-AKT and Bcl-2 coupled with reduced Bax, implying that PI3K-mediated attenuation of apoptosis facilitated tumor progression. Moreover, results from tumor xenograft mouse model experiments indicated that PI3K over-expression significantly promotes tumor growth in vivo. The present study confirmed the function of PI3K in accelerating the growth and invasive capacity of CMT, laying an experimental foundation for the exploration of PI3K-targeted therapies.