bladder carcinomas; matched adjacent non-tumor tissues; matched para-carcinomas; xenograft tumor tissues; lung sections
EJ; T24; 5673; BIU-87; SV-HUC-1; 293T; HUVECs
cell line-derived xenograft
VEGF/VEGFR (promotes); ERK (promotes); proliferation (promotes); migration (promotes); invasion (promotes); metastasis (promotes); EMT (promotes); angiogenesis (promotes); apoptosis (inhibits); ceRNA regulation (promotes); other pathway/process (promotes)
Back-Splice Junction PCR / divergent primers PCR; Sanger Sequencing; Microarray; RT-qPCR; FISH / smFISH; Clinical Sample Validation; Northern Blot; Transfection; CCK8; TUNEL; Wound Healing Assay; Transwell Assay; Tube Formation Assay; In Vivo Animal Model; H&E Staining; IF (Immunofluorescence); IHC (Immunohistochemistry); RIP (RNA Immunoprecipitation); Luciferase Reporter Assay; EdU Staining; Annexin V/PI Flow Cytometry; Western Blot; ELISA; Survival Analysis; Cohort Study; Bioinformatics Analysis
circRNA-MYLK levels were related to progression of stage and grade of bladder carcinoma; elevated circRNA-MYLK expression was associated with poor survival; proposed as a promising target for BC diagnosis and therapy.
circRNA-MYLK is upregulated in bladder carcinoma and its high expression correlates with advanced clinicopathological features and poor survival. It promotes BC proliferation, migration, invasion, angiogenesis, EMT, xenograft growth and metastasis by sponging miR-29a, increasing VEGFA, and activating VEGFA/VEGFR2 and downstream Ras/ERK signaling.
0.8743
Circular RNA MYLK as a competing endogenous RNA promotes bladder cancer progression through modulating VEGFA/VEGFR2 signaling pathway.
combined biological and clinical study