K Cui1, H Zhang, G-Z Wang. 1. Department of Pharmacy, Liaocheng Infectious Disease Hospital, Liaocheng, China. 15339949196@163.com.
Abstract
OBJECTIVE: To explore the mechanism underlying the effect of microRNA-483 (miR-483) in the progression of breast cancer (BC). PATIENTS AND METHODS: MiR-483 expression was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in both BC cells and tissue samples. The associations between miR-483 expression level and patients' overall survival rate were explored. Furthermore, cell proliferation assay and cell apoptosis assay were conducted, respectively. In addition, Western blot analysis and Luciferase assay were performed to explore the underlying mechanism. RESULTS: The expression level of miR-483 was significantly decreased in tumor samples compared to that in adjacent tissues, which was also associated with patients' overall survival time. Moreover, cell growth was promoted, and cell apoptosis was inhibited after miR-483 was knocked down in vitro. Furthermore, SOX3 acted as a direct target of miR-483, and the expression of SOX3 was negatively correlated with the expression of miR-483 in tumor tissues. CONCLUSIONS: These results suggested that miR-483 could suppress BC cell proliferation and promote BC cell apoptosis via targeting SOX3, which might be a potential therapeutic target in BC.
OBJECTIVE: To explore the mechanism underlying the effect of microRNA-483 (miR-483) in the progression of breast cancer (BC). PATIENTS AND METHODS: MiR-483 expression was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in both BC cells and tissue samples. The associations between miR-483 expression level and patients' overall survival rate were explored. Furthermore, cell proliferation assay and cell apoptosis assay were conducted, respectively. In addition, Western blot analysis and Luciferase assay were performed to explore the underlying mechanism. RESULTS: The expression level of miR-483 was significantly decreased in tumor samples compared to that in adjacent tissues, which was also associated with patients' overall survival time. Moreover, cell growth was promoted, and cell apoptosis was inhibited after miR-483 was knocked down in vitro. Furthermore, SOX3 acted as a direct target of miR-483, and the expression of SOX3 was negatively correlated with the expression of miR-483 in tumor tissues. CONCLUSIONS: These results suggested that miR-483 could suppress BC cell proliferation and promote BC cell apoptosis via targeting SOX3, which might be a potential therapeutic target in BC.