OBJECTIVE: This study was designed to investigate the expression level of circRNA_100876 in breast cancer (BC) tissues or cells, and to further explore whether it can promote cell metastasis and proliferative capacity via targeting microRNA- 361-3 p. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression of circRNA_100876 in 50 pairs of BC tissue specimens and corresponding adjacent ones, and the correlation between circRNA_100876 expression and prognosis of patients with BC was analyzed. Meanwhile, qRT-PCR was further performed to verify circRNA_100876 level in BC cell lines. In addition, circRNA_100876 knockdown model was constructed using lentivirus and transfected in BC cells. Subsequently, the impact of circRNA_100876 on BC cell function was analyzed using Cell Counting Kit-8 (CCK-8), transwell and clone formation assays. The interplay between circRNA_100876 and microRNA- 361-3 p was verified using the Luciferase reporter gene assay and cell reverse experiment. RESULTS: QRT-PCR results showed that circRNA_100876 level in BC tissues was conspicuously higher than that in the adjacent tissues, and the patients with distant metastasis had higher expression than those without. Moreover, patients with a high expression of circRNA_100876 had a relatively lower overall survival rate. Compared with the NC group, the cell proliferation and invasion ability of circRNA_100876 knockdown group was conspicuously decreased. QRT-PCR revealed that microRNA-361-3p and circRNA_100876 showed a negative correlation in the expression level of genes in BC tissues. In addition, the results of the Luciferase reporter gene assay confirmed that circRNA_100876 can be targeted by microRNA-361-3p through their binding site. CONCLUSIONS: High expression of circRNA_100876 is conspicuously positively relevant to poor prognosis of BC patients. Additionally, circRNA_100876 is able to promote BC metastasis as well as proliferative capacity by modulating microRNA-361-3p expression.
OBJECTIVE: This study was designed to investigate the expression level of circRNA_100876 in breast cancer (BC) tissues or cells, and to further explore whether it can promote cell metastasis and proliferative capacity via targeting microRNA- 361-3 p. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression of circRNA_100876 in 50 pairs of BC tissue specimens and corresponding adjacent ones, and the correlation between circRNA_100876 expression and prognosis of patients with BC was analyzed. Meanwhile, qRT-PCR was further performed to verify circRNA_100876 level in BC cell lines. In addition, circRNA_100876 knockdown model was constructed using lentivirus and transfected in BC cells. Subsequently, the impact of circRNA_100876 on BC cell function was analyzed using Cell Counting Kit-8 (CCK-8), transwell and clone formation assays. The interplay between circRNA_100876 and microRNA- 361-3 p was verified using the Luciferase reporter gene assay and cell reverse experiment. RESULTS: QRT-PCR results showed that circRNA_100876 level in BC tissues was conspicuously higher than that in the adjacent tissues, and the patients with distant metastasis had higher expression than those without. Moreover, patients with a high expression of circRNA_100876 had a relatively lower overall survival rate. Compared with the NC group, the cell proliferation and invasion ability of circRNA_100876 knockdown group was conspicuously decreased. QRT-PCR revealed that microRNA-361-3p and circRNA_100876 showed a negative correlation in the expression level of genes in BC tissues. In addition, the results of the Luciferase reporter gene assay confirmed that circRNA_100876 can be targeted by microRNA-361-3p through their binding site. CONCLUSIONS: High expression of circRNA_100876 is conspicuously positively relevant to poor prognosis of BC patients. Additionally, circRNA_100876 is able to promote BC metastasis as well as proliferative capacity by modulating microRNA-361-3p expression.