Original Article
Aspirin inhibits the proliferation of canine mammary gland tumor cells in vitro and in vivo
Abstract
Background: Aspirin (acetylsalicylic acid), a non-steroidal anti-inflammatory drug (NSAID), is widely used to manage pain, arthritis, and cardiovascular diseases. Recent studies have shown that Aspirin could inhibit the growth of various human cancer cells in vitro and in vivo. The beneficial impact of Aspirin on human breast cancer has not been confirmed, and the precise mechanism of anti-tumor effect of Aspirin is largely unknown. Moreover, there is no evidence for the anti-tumor effect of Aspirin on canine mammary gland tumors (CMGT) cells. In this study, we investigated the effects of Aspirin on CMGT cells and the underlying mechanisms
Methods: Cell proliferation was determined by cell viability assay and clone formation assay. Changes of apoptosis after Aspirin treatment were determined by Annexin-V-FITC apoptosis assay using flow-cytometry analysis, western blot assay for PARP, Bcl-2 and BAX expression. Effects of Aspirin on cell cycle arrest regulation were determined by flow-cytometry analysis, western blot assay for cyclin D1, CDK4, E2F1 and p21 expression. CMGT xenograft model was used to validate the anti-tumor effects of Aspirin in vivo.
Results: We found that Aspirin not only effectively suppressed the proliferation and colony formation of CMGT cells in vitro, but also inhibited the tumor growth in vivo. Aspirin selectively induce apoptosis of metastatic CMGT cells, and our investigation showed that Aspirin could inhibit cell cycle progression at the G0/G1 checkpoint leading to decreased viability of the cells.
Conclusions: Our results demonstrate that Aspirin efficiently inhibits the proliferation of CMGT cells and suggest that Aspirin might be a potential chemotherapy drug for CMGT.
Methods: Cell proliferation was determined by cell viability assay and clone formation assay. Changes of apoptosis after Aspirin treatment were determined by Annexin-V-FITC apoptosis assay using flow-cytometry analysis, western blot assay for PARP, Bcl-2 and BAX expression. Effects of Aspirin on cell cycle arrest regulation were determined by flow-cytometry analysis, western blot assay for cyclin D1, CDK4, E2F1 and p21 expression. CMGT xenograft model was used to validate the anti-tumor effects of Aspirin in vivo.
Results: We found that Aspirin not only effectively suppressed the proliferation and colony formation of CMGT cells in vitro, but also inhibited the tumor growth in vivo. Aspirin selectively induce apoptosis of metastatic CMGT cells, and our investigation showed that Aspirin could inhibit cell cycle progression at the G0/G1 checkpoint leading to decreased viability of the cells.
Conclusions: Our results demonstrate that Aspirin efficiently inhibits the proliferation of CMGT cells and suggest that Aspirin might be a potential chemotherapy drug for CMGT.
