| Expression pattern: |
UP |
| Associated gene: |
HMGB2, Ago2, MMP-1, MMP-13, cleaved caspase-3, cytochrome C, p-NF-kappaB, IL-6, IL-8, TNF-alpha |
| Associated microRNA: |
miR-421 |
| Biological function: |
circSLTM promotes OA chondrocyte apoptosis and inflammation, reduces chondrocyte viability, increases LDH release and ROS production, and aggravates cartilage destruction; circSLTM knockdown ameliorates apoptosis, inflammation, and cartilage damage in OA models. |
| Molecular mechanism: |
circSLTM acts as a competing endogenous RNA for miR-421, thereby regulating HMGB2 expression and promoting p-NF-kappaB-related inflammatory signaling and apoptosis in OA chondrocytes. |
| Biological pathway or process: |
apoptosis (promotes); inflammation (promotes); NF-kappaB (promotes); proliferation (inhibits); ceRNA regulation (other); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Bioinformatics Analysis; RIP (RNA Immunoprecipitation); Luciferase Reporter Assay; Transfection; CCK8; Annexin V/PI Flow Cytometry; ELISA; Western Blot; In Vivo Animal Model; H&E Staining; IF (Immunofluorescence); TUNEL |
| Clinical significance: |
circSLTM may serve as a potential molecular target for OA therapy. |
| Description: |
circSLTM is up-regulated in IL-1beta-induced OA chondrocytes and in OA rat cartilage/knee tissue models. It functions as a miR-421-competing endogenous RNA to regulate HMGB2, thereby promoting NF-kappaB-related inflammation, ROS production, apoptosis, and cartilage damage; knockdown of circSLTM alleviates OA-like injury in vitro and in vivo. |
| Confidence score: |
0.6279 |