| Expression pattern: |
UP |
| Associated gene: |
PKM2, EIF4A3, CCL3, NF-kappaB, p65/NF-kappaB |
| Associated microRNA: |
- |
| Biological function: |
Promotes ESCC cell proliferation, migration, invasion, tumor growth and metastasis; increases CCL3 secretion. |
| Molecular mechanism: |
circPRKAR1B binds PKM2, enhances NF-kappaB (p65) phosphorylation, and promotes NF-kappaB-mediated CCL3 secretion; EIF4A3 binds flanking sequences to promote circPRKAR1B biogenesis. |
| Biological pathway or process: |
NF-kappaB (promotes); proliferation (promotes); migration (promotes); invasion (promotes); metastasis (promotes); other pathway/process (promotes) |
| Detected method: |
Q
H
|
| Validation methods: |
RT-qPCR; FISH / smFISH; Nuclear-Cytoplasmic Fractionation; Back-Splice Junction PCR / divergent primers PCR; Sanger Sequencing; RNase R Treatment; Actinomycin D / DRB Stability Assay; Microarray; ELISA; Western Blot; RNA Pull-Down; Bioinformatics Analysis; Transfection; CCK8; Colony Formation Assay; Transwell Assay; Wound Healing Assay; In Vivo Animal Model; IHC (Immunohistochemistry); Survival Analysis; Cohort Study; H&E Staining |
| Clinical significance: |
circPRKAR1B is significantly elevated in ESCC tissues and high circPRKAR1B levels are linked to lower overall survival; circPRKAR1B expression is an independent prognostic factor. |
| Description: |
circPRKAR1B is upregulated in ESCC tissues/cells and promotes proliferation, migration, invasion, and in vivo tumor growth/metastasis. It binds PKM2 to activate NF-kappaB signaling and increase CCL3 secretion, and its biogenesis is promoted by EIF4A3 binding to flanking sequences. High circPRKAR1B expression is associated with poor overall survival and adverse clinicopathologic features in ESCC. |
| Confidence score: |
0.8637 |