Abstract
The main problem in breast cancer treatment is the recurrence of tumor growth and metastases. Previous studies have suggested that Paclitaxel is widely used to treat various cancers. The present study analyzed the potential signaling pathway of Paclitaxel-inhibited breast cancer metastasis. It was demonstrated that Paclitaxel treatment significantly inhibited growth of breast cancer cell lines including MCF-7 and SKBR3 cells. Results demonstrated that Paclitaxel significantly inhibited breast cancer cell migration and invasion. Results additionally demonstrated that Paclitaxel treatment suppressed Aurora kinase and cofilin-1 activity in breast cancer cells. The potential mechanism indicated that activation of Aurora kinase activity stimulated cofilin-1 activity, which canceled Paclitaxel-inhibited growth and aggressiveness of breast cancer cells. An in vivo assay revealed that Paclitaxel treatment significantly inhibited breast cancer growth. Immunohistochemistry demonstrated that Paclitaxel treatment increased apoptosis of tumor cells in tumor tissue. Notably, Aurora kinase and cofilin-1 activity were downregulated by Paclitaxel in tumor tissues. In conclusion, these results indicated that Paclitaxel inhibited breast cancer cell growth and metastasis via suppression of Aurora kinase-mediated cofilin-1 activity, suggesting Paclitaxel may be an efficient anticancer agent for the treatment of this disease.