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Abstract
Aim
Cervical cancer (CC) is the fourth most common cancer among women worldwide. We aimed to explore the role of hsa_circ_000543 played in CC.
Methods
The hsa_circ_000543 expressions in CC tissues and cells were measured by qRT-PCR. The correlation of hsa_circ_000543 expression and the clinical features of CC patients were analyzed by SPSS 20.0. The up- or down-regulated plasmids of hsa_circ_000543 were respectively transfected into CC cells. Cell proliferation, apoptosis and colony formation were detected through CCK-8 assay, flow cytometry and cell colony formation assay, respectively. The cell migration and invasion were evaluated by Transwell assay. The underlying molecular mechanism of hsa_circ_000543 was studied by bioinformatic prediction tools and luciferase reporter assay. Rescue experiments were performed to validate the regulation mechanism of hsa_circ_000543/miR-567/ZNF268 axis in CC.
Results
Hsa_circ_000543 was over-expressed in CC tissues and cells. The high expression of hsa_circ_000543 indicated poor prognosis of CC patients. Hsa_circ_000543 promoted cell proliferation, colony formation, migration and invasion, as well as inhibited cell apoptosis in CC cells. Hsa_circ_000543 directly targeted miR-567/ZNF268 in CC cell lines. In CC tumor tissues and cells, the hsa_circ_000543 expression was negatively correlated with miR-567 expression and showed a positive correlation with ZNF268 expression. The rescue experiments revealed that hsa_circ_000543 mediated cell proliferation, apoptosis, colony formation, migration and invasion of CC cells via regulating miR-567/ZNF268 axis.
Conclusion
Hsa_circ_000543 regulated CC cell activities through binding miR-567 and therefore enhancing ZNF268 expression.
Disclosure
The authors declare no conflict of interest.