| Expression pattern: |
UP |
| Associated gene: |
IGF2BP2, IGF2BP1, IGF2BP3, NRARP, ESM1, METTL3, METTL14 |
| Associated microRNA: |
- |
| Biological function: |
Promotes endothelial tip cell specialization, endothelial migration and sprouting, retinal and choroidal pathological angiogenesis, retinal vascular leakage, and neovascular tuft formation. |
| Molecular mechanism: |
Acts as an m6A-dependent scaffold that interacts with IGF2BP2 and promotes formation of circMET/IGF2BP2/NRARP or ESM1 complex, thereby stabilizing NRARP and ESM1 mRNAs; it does not act as a miRNA sponge in HRVECs. |
| Biological pathway or process: |
angiogenesis (promotes); migration (promotes); mRNA stability (promotes); m6A modification (other); Notch (other); Wnt/beta-catenin (other); VEGF/VEGFR (promotes); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; FISH / smFISH; IF (Immunofluorescence); Clinical Sample Validation; RIP (RNA Immunoprecipitation); RNA Pull-Down; MeRIP / MeRIP-seq; Transfection; Transwell Assay; Western Blot; ELISA; In Vivo Animal Model; Bioinformatics Analysis |
| Clinical significance: |
circMET is upregulated in vitreous samples of patients with DME or PDR, correlates with severity of retinal vascular dysfunction, is reduced by anti-VEGF treatment, and is proposed as a diagnostic/prognostic biomarker and therapeutic target for ocular vascular disease. |
| Description: |
circMET is upregulated in mouse models of ocular pathological angiogenesis and in vitreous samples from patients with diabetic retinal vascular disease. It promotes endothelial tip cell specialization, endothelial sprouting, migration, and pathological angiogenesis by forming an m6A-dependent circMET/IGF2BP2/NRARP or ESM1 complex that stabilizes NRARP and ESM1 expression. The study proposes circMET as a biomarker and therapeutic target for proliferative retinopathies and other neovascular diseases. |
| Confidence score: |
0.7519 |