Abstract:
BACKGROUND:Breast cancer (BC) is a heterogeneous malignant tumor that threatens the health of women worldwide. Hsa_circRNA_0000518 (circ_0000518) has been revealed to be upregulated in BC tissues. However, the role and mechanism of circ_0000518 in BC are indistinct. METHODS:Quantitative real-time polymerase chain reaction (qRT-PCR) was implemented to detect the levels of circ_0000518, microRNA (miR)-326, and fibroblast growth factor receptor 1 (FGFR1) mRNA in BC tissues and cells. Cell counting kit-8 (CCK-8), colony formation, flow cytometry, and transwell assays were executed to estimate BC cell proliferation, cell cycle progression, apoptosis, migration, and invasion. The relationship between circ_0000518 or FGFR1 and miR-326 was verified by dual-luciferase reporter and/or RNA immunoprecipitation (RIP) assays. The role of circ_0000518 in vivo was confirmed by xenograft assay. RESULTS:Circ_0000518 and FGFR1 were upregulated while miR-326 was downregulated in BC tissues and cells. Circ_0000518 silencing impeded tumor growth in vivo and induced cell cycle arrest, apoptosis, cured proliferation, colony formation, migration, and invasion of BC cells in vitro. Circ_0000518 regulated FGFR1 expression via competitively binding to miR-326 in BC cells. MiR-326 inhibitor reversed the inhibitory influence of circ_0000518 knockdown on the malignant behaviors of BC cells. FGFR1 overexpression abolished miR-326 mimic-mediated influence on the malignant behaviors of BC cells. CONCLUSIONS:Circ_0000518 facilitated BC development via regulation of the miR-326/FGFR1 axis, suggesting that circ_0000518 might be a promising target for BC treatment.
journal_name
Thorac Cancerjournal_title
Thoracic cancerauthors
Jiang J,Lin H,Shi S,Hong Y,Bai X,Cao Xdoi
10.1111/1759-7714.13641subject
Has Abstractpub_date
2020-11-01 00:00:00pages
3181-3192issue
11eissn
1759-7706issn
1759-7714journal_volume
11pub_type
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