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Breast cancer is one of the most common metastatic tumor types. Reports have suggested that Tunicamycin may inhibit the aggressiveness of cancer cells by promoting their apoptosis. In the present study, the inhibitory effects of Tunicamycin were investigated and the potential molecular mechanism underlying the Tunicamycin-inhibited growth and aggressiveness of breast cancer cells was explored. In vitro assays demonstrated that Tunicamycin significantly inhibited growth and arrested the cell cycle of breast cancer cells in a dose-dependent manner, compared with control cells. Results revealed that Tunicamycin treatment suppressed the migration and invasion of breast cancer cells. Significantly increased apoptosis of breast cancer cells was observed subsequent to Tunicamycin treatment, as compared with control cells. Mechanism analysis demonstrated that Tunicamycin inhibited the protein kinase B (Akt) and nuclear factor-κB (NF-κB) signaling pathways, whilst Akt overexpression significantly cancelled out the Tunicamycin-inhibited growth and aggressiveness of breast cancer cells, as compared with control cells. In vivo assays revealed that Tunicamycin treatment significantly inhibited tumor growth and significantly prolonged the survival of tumor-bearing mice, compared with the PBS-treated group. In conclusion, these results indicate that Tunicamycin may inhibit the growth and aggressiveness of breast cancer cells via regulation of the Akt/NF-κB signaling pathway.

Tunicamycin suppresses breast cancer cell growth and metastasis via regulation of the protein kinase B/nuclear factor-κB signaling pathway