| Expression pattern: |
UP |
| Associated gene: |
Dicer, TRBP |
| Associated microRNA: |
miR-195 |
| Biological function: |
inhibits proliferation and delays injury-induced regeneration/repair of the intestinal epithelium; protects mucosa against colitis when deleted |
| Molecular mechanism: |
modulates miR-195 (Cdr1as/miR-195 axis) by stabilizing pre-miR-195 and affecting miRNA biogenesis/processing (Dicer/TRBP), thereby regulating epithelial repair and organoid growth |
| Biological pathway or process: |
proliferation (inhibits); migration (inhibits); apoptosis (other); ceRNA regulation (other) |
| Detected method: |
Q
H
|
| Validation methods: |
RNase R Treatment; RT-qPCR; Nuclear-Cytoplasmic Fractionation; FISH / smFISH; Microarray; Transfection; Actinomycin D / DRB Stability Assay; BrdU; TUNEL; In Vivo Animal Model; H&E Staining; Western Blot; IF (Immunofluorescence) |
| Clinical significance: |
Cdr1as is increased in human intestinal mucosa from patients with UC, CD, and sepsis and is associated with mucosal injury/erosions, inflammation, and delayed healing |
| Description: |
Cdr1as is induced in injured/inflamed intestinal mucosa (mouse colitis/septic stress and human IBD/sepsis) and acts as a negative regulator of intestinal epithelial proliferation and wound repair. Mechanistically, it regulates the Cdr1as/miR-195 axis by affecting miR-195 biogenesis and stabilizing pre-miR-195, thereby impairing epithelial repair and organoid growth; genetic deletion of Cdr1as improves regeneration and protects against colitis. |
| Confidence score: |
0.6566 |