Background: Breast cancer (BCa) is an overwhelming malignant tumor mainly in women globally. Circular RNAs (circRNAs) are a special type of noncoding RNAs involved in competing endogenous RNA (ceRNA) network, a classic molecular mechanism of the tumorigenesis of human cancers, including BCa. Here, we intended to explore the role and mechanism of () in BCa cells.

Methods: Expression of , () and () was measured by real time-quantitative PCR and Western blotting. Cell growth was measured by cell counting kit-8, colony formation assay and flow cytometry method. Cell migration and invasion were assessed by transwell assays and Western blotting. Tumor growth was determined by xenograft models. The direct interaction among , and was confirmed by dual-luciferase reporter assay and RNA pull-down assay.

Results: was upregulated in BCa tumors and cell lines (T47D, MCF7, MDA-MB-231, BT549, and SKBR3), and high expression was associated with poor overall survival. Blocking suppressed cell viability, colony formation, migration and invasion, but promoted cell cycle arrest and apoptosis rate in MDA-MB-231 and MCF7 cells. could directly regulate expression, and was a novel target for . Moreover, the anti-tumor role of silencing was abrogated by downregulation or restoration. Notably, tumor growth of MDA-MB-231 cells in mice was restrained by deletion.

Conclusion: knockdown could suppress cell growth, migration and invasion both in vitro and in vivo through regulating pathway.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457856PMC
http://dx.doi.org/10.2147/CMAR.S251666DOI Listing

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