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circ-MYBL2 Serves As A Sponge For miR-361-3p Promoting Cervical Cancer Cells Proliferation And Invasion
BACKGROUND: Circular RNAs (circRNAs) have been considered as a key regulator in tumor carcinogenesis. However, the roles and underlying mechanisms of circRNAs in cervical cancer (CC) remain largely unknown. In this study, we explored the effects of circ-MYBL2 (hsa_circ_0060467) on CC progression. ME...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6877451/ https://www.ncbi.nlm.nih.gov/pubmed/31819492 http://dx.doi.org/10.2147/OTT.S218976 |
Sumario: | BACKGROUND: Circular RNAs (circRNAs) have been considered as a key regulator in tumor carcinogenesis. However, the roles and underlying mechanisms of circRNAs in cervical cancer (CC) remain largely unknown. In this study, we explored the effects of circ-MYBL2 (hsa_circ_0060467) on CC progression. METHODS: Levels of circ-MYBL2 and miR-361-3p were examined by qRT-PCR. CCK-8 assay, colony formation assay and transwell invasion assay were used to determine the roles of circ-MYBL2 in CC. Dual-luciferase reporter and RNA pull down assays were employed to verify the relationship between circ-MYBL2 and miR-361-3p. RESULTS: We showed that the expression of circ-MYBL2 was significantly upregulated and positively associated with advanced FIGO stage, larger tumor size, lymph node metastasis, and poor prognosis in CC patients. Function assays revealed that circ-MYBL2 inhibition suppressed CC cells’ proliferation, invasion and epithelial–mesenchymal transition (EMT) processes. In mechanism, miR-361-3p was identified as a direct target of circ-MYBL2, rescue assays showed that miR-361-3p suppression reversed the effects of si-circ-MYBL2 on CC cells’ progression. CONCLUSION: Our findings suggested that circ-MYBL2 promoted CC progression by regulating miR-361-3p expression, which provided a novel therapeutic target for the treatment of CC patients. |
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