CircFAM64A enhances cellular processes in triple-negative breast cancer by targeting the miR-149-5p/CDT1 axis.

Triple-negative breast cancer (TNBC) is a breast cancer subtype without targeted treatment options. Accumulating evidence has demonstrated the roles of circular RNAs in cancer. This study aimed to investigate the expression and function of circFAM64A in TNBC. The GSE101124 dataset from the GEO database was examined to identify the differentially expressed circular RNAs in TNBC. RT-qPCR and western blot analyses were performed to measure gene expression. TNBC cell proliferation, migration, invasion, and cell cycle were assessed using cell counting kit-8, EdU, flow cytometry, wound healing, and transwell invasion experiments. Bioinformatics analysis, RIP, RNA pulldown, and luciferase reporter assays were used to investigate the regulatory mechanism of circFAM64A. In this study, CircFAM64A expression was significantly upregulated in TNBC tissues and cells compared with normal tissues and cells. Overexpression of circFAM64A increased the proliferative, migratory, and invasive capacities of TNBC cells and promoted cell cycle progression. Mechanistically, circFAM64A acted as a molecular sponge for miR-149-5p, and miR-149-5p directly targeted the Cdc10-dependent transcript 1 (CDT1) 3'UTR. Moreover, the high expression of CDT1 is associated with a poor prognosis in patients with breast cancer. Rescue experiments demonstrated that circFAM64A sponged miR-149-5p to increase CDT1 expression, thereby promoting cellular processes in TNBC. Overall, CircFAM64A plays an oncogenic role in TNBC by interacting with miR-149-5p to increase CDT1 expression.