| Expression pattern: |
DN |
| Associated gene: |
TGF-beta1, HYBID, HAS2 |
| Associated microRNA: |
hsa-miR-29b-3p |
| Biological function: |
Promotes hyaluronan synthesis/accumulation in chondrocytes and plays a protective role against OA progression; suppresses inflammatory responses in IL-1beta-treated chondrocytes. |
| Molecular mechanism: |
Acts as a miRNA sponge (ceRNA) for hsa-miR-29b-3p to upregulate TGF-beta1, thereby regulating HA metabolism (promoting HA anabolism and suppressing catabolism) and affecting HYBID and HAS2 expression. |
| Biological pathway or process: |
ceRNA regulation (promotes); other pathway/process (other) |
| Detected method: |
Q
S
|
| Validation methods: |
RNA-seq; RT-qPCR; Back-Splice Junction PCR / divergent primers PCR; Sanger Sequencing; Bioinformatics Analysis; Luciferase Reporter Assay; Transfection; ELISA; Western Blot; IHC (Immunohistochemistry); Clinical Sample Validation |
| Clinical significance: |
circHYBID may serve as a potential target for OA therapy. |
| Description: |
In osteoarthritis cartilage and IL-1beta-stimulated human chondrocytes, circHYBID is down-regulated. circHYBID overexpression increases HA accumulation and modulates HA-metabolism enzymes (decreases HYBID and restores HAS2). Mechanistically, it sponges hsa-miR-29b-3p to upregulate TGF-beta1, forming a circHYBID/miR-29b-3p/TGF-beta1 axis that regulates HA metabolism and may be therapeutically relevant in OA. |
| Confidence score: |
0.8082 |