BC tissues; xenografts
SK-BR-3; BT-549; MCF-10A; 293T
cell line-derived xenograft
glycolysis (promotes); proliferation (promotes); migration (promotes); invasion (promotes); cell cycle (promotes); ceRNA regulation (promotes)
Back-Splice Junction PCR / divergent primers PCR; RNase R Treatment; Sanger Sequencing; Actinomycin D / DRB Stability Assay; RT-qPCR; FISH / smFISH; Nuclear-Cytoplasmic Fractionation; Clinical Sample Validation; RIP (RNA Immunoprecipitation); RNA Pull-Down; Luciferase Reporter Assay; Transfection; CCK8; EdU Staining; Cell Cycle Assay; Transwell Assay; In Vivo Animal Model; IHC (Immunohistochemistry); Western Blot; Bioinformatics Analysis
High circANKRD17 expression in BC patients was associated with higher SUV max on 18 F-FDG PET/CT, and circANKRD17 was suggested as a promising therapeutic target to interrupt cancerous glycolysis.
circANKRD17 is up-regulated in breast cancer cells and promotes glycolysis and malignant phenotypes including proliferation, migration, invasion, and cell-cycle progression. Mechanistically, circANKRD17 acts as a cytoplasmic sponge for miR-143, relieving repression of HK2 and increasing glycolytic activity, including glucose consumption, lactate production, and 18 F-FDG uptake. In patient BC tissues, high circANKRD17 expression is associated with higher SUV max on 18 F-FDG PET/CT, supporting its potential as a therapeutic target for cancerous glycolysis.
0.8793
CircANKRD17 promotes glycolysis by inhibiting miR-143 in breast cancer cells.
combined biological and clinical study