| Expression pattern: |
DN |
| Associated gene: |
ITCH, Ago2, Dvl2, beta-catenin, c-Myc, cyclin D1 |
| Associated microRNA: |
miR-17, miR-214 |
| Biological function: |
inhibits proliferation; inhibits migration; inhibits invasion; suppresses tumor growth/tumourigenesis |
| Molecular mechanism: |
Acts as a miRNA sponge (ceRNA) for miR-17 (and miR-214), increasing linear ITCH expression; ITCH then suppresses canonical Wnt/beta-catenin signaling (via Dvl2), reducing Wnt target genes (c-Myc, cyclin D1). |
| Biological pathway or process: |
Wnt/beta-catenin (inhibits); proliferation (inhibits); migration (inhibits); invasion (inhibits); ceRNA regulation (other) |
| Detected method: |
Q
|
| Validation methods: |
divergent primers PCR; RNase R Treatment; RT-qPCR; Clinical Sample Validation; RIP (RNA Immunoprecipitation); RNA Pull-Down; Luciferase Reporter Assay; Transfection; CCK8; Colony Formation Assay; Transwell Assay; In Vivo Animal Model; IHC (Immunohistochemistry); Western Blot; Survival Analysis; Bioinformatics Analysis |
| Clinical significance: |
High cir-ITCH expression is associated with longer overall survival; cir-ITCH may serve as a prognostic marker; cir-ITCH is lower in metastatic (lymph node metastasis) gastric cancer tissues. |
| Description: |
cir-ITCH is down-regulated in gastric cancer and functions as a tumor suppressor by inhibiting proliferation, migration, invasion and in vivo tumor growth. Mechanistically, cir-ITCH sponges miR-17 (also binds miR-214), elevates linear ITCH, and suppresses canonical Wnt/beta-catenin signaling (Dvl2/beta-catenin and Wnt target genes such as c-Myc and cyclin D1). High cir-ITCH expression is associated with better overall survival. |
| Confidence score: |
0.859 |