bladder cancer tissues; adjacent normal tissues; peripheral blood; xenograft tissues
BIU87; UMUC3; T24; 5637; 253 J; RT4; SV-HUC-1; HEK293T; J82
cell line-derived xenograft
JAK/STAT (promotes); proliferation (promotes); invasion (promotes); immune regulation (promotes); ceRNA regulation (promotes); other pathway/process (promotes)
Bioinformatics Analysis; Back-Splice Junction PCR / divergent primers PCR; Sanger Sequencing; RNase R Treatment; RT-qPCR; Nuclear-Cytoplasmic Fractionation; FISH / smFISH; Clinical Sample Validation; Cohort Study; Survival Analysis; Transfection; CCK8; EdU Staining; Colony Formation Assay; Transwell Assay; ELISA; RNA-seq; RNA Pull-Down; RIP (RNA Immunoprecipitation); Luciferase Reporter Assay; Western Blot; In Vivo Animal Model; IHC (Immunohistochemistry); Flow Cytometry(Non-apoptosis/cycle)
High circFAM64A(3) expression was associated with poor prognosis, worse OS and PFS, and a tendency toward muscle invasive bladder cancer.
CircFAM64A(3), also identified as hsa_circ_0041732, is up-regulated in bladder cancer and high expression is associated with poor prognosis. Functionally, it promotes bladder cancer proliferation and invasion and suppresses CD8+ T cell-mediated antitumor killing. Mechanistically, hypoxia-induced HIF-1alpha promotes circFAM64A(3) transcription, and circFAM64A(3) sponges miR-149-5p to increase IL-6, activate the JAK/STAT pathway, and elevate PD-L1 expression.
0.8942
CircFAM64A(3) promoted bladder cancer proliferation and inhibited CD8 + T cell via sponging to miR-149-5p and activated IL-6/JAK/STAT pathway.
combined biological and clinical study