| Expression pattern: |
DN |
| Associated gene: |
DOHH, Dohh mRNA, AGO2, NF-kappaB p65 |
| Associated microRNA: |
miR-10b-5p |
| Biological function: |
Promotes cementoblast differentiation and mineralization; mitigates the inhibitory effects of TNF-alpha on cementoblast differentiation and mineralization under inflammatory conditions. |
| Molecular mechanism: |
ceRNA mechanism: circHIPK3 sponges miR-10b-5p to upregulate DOHH expression and activate the NF-kappaB pathway. |
| Biological pathway or process: |
NF-kappaB (promotes); ceRNA regulation (promotes); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
Back-Splice Junction PCR / divergent primers PCR; Sanger Sequencing; Actinomycin D / DRB Stability Assay; RT-qPCR; RNA-seq; Nuclear-Cytoplasmic Fractionation; RIP (RNA Immunoprecipitation); RNA Pull-Down; Luciferase Reporter Assay; Transfection; Western Blot; In Vivo Animal Model; H&E Staining; IHC (Immunohistochemistry); Bioinformatics Analysis |
| Clinical significance: |
could be an effective therapeutic target for treating cementum damage |
| Description: |
This study identifies murine circHIPK3 as a positive regulator of cementoblast differentiation and mineralization. Under inflammatory conditions such as TNF-alpha exposure and apical periodontitis, circHIPK3 is down-regulated, and restoring circHIPK3 partly rescues impaired cementoblast differentiation. Mechanistically, circHIPK3 functions as a ceRNA that sponges miR-10b-5p, increases DOHH expression, and activates the NF-kappaB pathway. |
| Confidence score: |
0.8462 |