Background: Breast cancer is one of the most common and malignant tumors in the world. Nowadays more attention has been garnered in pristimerin anti-cancer effects. Here, we illustrate the function and regulatory mechanism of pristimerin in breast cancer therapy.
Materials and methods: Breast cancer cell lines MCF-7, MDA-MB-231, and 4T1 were used. Cell Counting Kit-8 (CCK-8) assay was performed to evaluate proliferation viability of breast cancer cells under pristimerin treatment. Wound healing assay was used to examine the migration ability, cell cycle, and cell apoptosis detection were tested by flow cytometry. Bioinformatic analysis was used to find the underlying molecular and gene connected with pristimerin and breast cancer survival. Finally, we used transfection and real-time polymerase chain reaction analysis to confirm the mechanism.
Results: We observed that pristimerin inhibited breast cancer cell viability, migration, and cell cycle, meanwhile induced cell apoptosis. In addition, under pristimerin treatment, miR-542-5p was up-regulated while DUB3 was down-regulated. Furthermore, bioinformatics analysis showed higher expression of DUB3 in breast cancer compared with normal tissue, also with poor prognosis. Overexpression miR-542-5p in breast cancer cells leads to a decrease in DUB3 level. The effect was obviously post pristimerin treatment and miR-542-5p overexpression.
Conclusion: Pristimerin inhibited breast cancer progression through DUB3 expression via a canonical miRNA-mediated mechanism.
Keywords: AGO2; DUB3; anti-cancer; breast cancer; miRNA; pristimerin.
© 2020 Cheng et al.