| Expression pattern: |
DN |
| Associated gene: |
Bcl-2, Bax, Caspase-9, TNF-alpha, IL-6, IL-8, IL-10 |
| Associated microRNA: |
miR-7 |
| Biological function: |
ciRS-7 regulates chondrocyte proliferation, apoptosis and inflammation in OA; reduced ciRS-7 enhances IL-1beta-induced inflammatory cytokine release and apoptosis, whereas increased ciRS-7 suppresses apoptosis-related Bax and cleaved caspase-9 and promotes Bcl-2 expression. |
| Molecular mechanism: |
ciRS-7 acts through the ciRS-7/miR-7 axis, functioning as an endogenous competitive RNA inhibitor or sponge of miR-7, thereby regulating inflammatory cytokine release and apoptosis-associated proteins in IL-1beta-induced OA chondrocytes. |
| Biological pathway or process: |
proliferation (promotes); apoptosis (inhibits); inflammation (inhibits); ceRNA regulation (other) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Clinical Sample Validation; Transfection; MTT; ELISA; Annexin V/PI Flow Cytometry; Western Blot |
| Clinical significance: |
ciRS-7 was significantly lower in OA patients than in healthy subjects and may provide novel insights into treatments for OA. |
| Description: |
This study found that human ciRS-7 is down-regulated in blood/plasma from OA patients and in IL-1beta-induced chondrocytes. Functionally, ciRS-7 appears protective in OA model chondrocytes: knockdown promotes inflammatory cytokine release and apoptosis, whereas ciRS-7 overexpression suppresses Bax and cleaved caspase-9 and promotes Bcl-2. The proposed mechanism is regulation through the ciRS-7/miR-7 axis. |
| Confidence score: |
0.5414 |