| Expression pattern: |
DN |
| Associated gene: |
ITCH, Dvl2, beta-catenin, Wnt3a, c-Myc |
| Associated microRNA: |
miR-7, miR-17, miR-214, miR-216b, miR-128 |
| Biological function: |
Acts as a tumor suppressor in ESCC by inhibiting proliferation/viability, inducing G1 arrest, and suppressing tumor growth. |
| Molecular mechanism: |
ceRNA/miRNA sponge mechanism: cir-ITCH sponges miRNAs (e.g., miR-7/miR-17/miR-214 etc.) shared with ITCH 3′UTR, increases ITCH expression, promotes ubiquitination and degradation of phosphorylated Dvl2, thereby inhibiting canonical Wnt/beta-catenin signaling and downstream targets such as c-Myc. |
| Biological pathway or process: |
Wnt/beta-catenin (inhibits); proliferation (inhibits); cell cycle (inhibits); ceRNA regulation (promotes) |
| Detected method: |
Q
|
| Validation methods: |
divergent primers PCR; RNase R Treatment; RT-qPCR; Clinical Sample Validation; Bioinformatics Analysis; Luciferase Reporter Assay; Actinomycin D / DRB Stability Assay; Transfection; Western Blot; CCK8; Colony Formation Assay; Cell Cycle Assay; In Vivo Animal Model |
| Clinical significance: |
cir-ITCH is down-regulated in ESCC tumor tissues compared with paired adjacent tissues in large cohorts (Suzhou and Guangzhou). |
| Description: |
cir-ITCH is down-regulated in ESCC tissues and functions as a tumor suppressor. It sponges multiple miRNAs to increase ITCH, promoting degradation of phosphorylated Dvl2 and thereby inhibiting Wnt/beta-catenin signaling, reducing c-Myc and suppressing proliferation and tumor growth. |
| Confidence score: |
0.779 |