| Expression pattern: |
DN |
| Associated gene: |
beta-catenin, AKT, p-AKT, mTOR, p-mTOR |
| Associated microRNA: |
miR-17 / hsa-miR-17-5p |
| Biological function: |
Inhibits proliferation/viability, migration, and invasion of prostate cancer cells (tumor-suppressive role). |
| Molecular mechanism: |
Reciprocal inhibition with miR-17 and suppression of Wnt/beta-catenin and PI3K/AKT/mTOR pathway activity (reduced beta-catenin, p-AKT, p-mTOR) upon cir-ITCH overexpression; proposed miR-17 sponging. |
| Biological pathway or process: |
proliferation (inhibits); migration (inhibits); invasion (inhibits); Wnt/beta-catenin (inhibits); PI3K/AKT/mTOR (inhibits); ceRNA regulation (other) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Clinical Sample Validation; Transfection; CCK8; Wound Healing Assay; Transwell Assay; Western Blot; Bioinformatics Analysis |
| Clinical significance: |
Potential therapeutic target for prostate cancer, especially castration-resistant prostate cancer. |
| Description: |
cir-ITCH (hsa_circ_0001141) is down-regulated in prostate cancer tissues and cell lines. Its overexpression suppresses PCa cell viability/proliferation, migration and invasion, and it negatively interacts with miR-17 while inhibiting Wnt/beta-catenin and PI3K/AKT/mTOR signaling activity, suggesting therapeutic potential for CRPC. |
| Confidence score: |
0.5732 |