| Expression pattern: |
DN |
| Associated gene: |
- |
| Associated microRNA: |
miR-9-3p |
| Biological function: |
circFOXP1 suppresses apoptosis, inflammation, and oxidative stress, promotes proliferation in H/R-stressed AC16 cells, and attenuates heart injury in the AMI mouse model. |
| Molecular mechanism: |
circFOXP1 acts through miR-9-3p, with luciferase reporter evidence that miR-9-3p directly binds circFOXP1 and reverses circFOXP1 effects on H/R AC16 cells and the AMI model. |
| Biological pathway or process: |
apoptosis (inhibits); proliferation (promotes); inflammation (inhibits); ceRNA regulation (other); p53 signaling (other); PI3K/AKT (other); AMPK (other); Hedgehog (other); other pathway/process (inhibits) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Luciferase Reporter Assay; Transfection; CCK8; Annexin V/PI Flow Cytometry; Flow Cytometry（Non-apoptosis/cycle）; In Vivo Animal Model; ELISA; ROC Analysis; Bioinformatics Analysis; Clinical Sample Validation |
| Clinical significance: |
circFOXP1 was decreased in AMI patients and may serve as a diagnostic marker; ROC AUC was 0.881 with sensitivity 0.930 and specificity 0.785. |
| Description: |
circFOXP1 is downregulated in acute myocardial infarction patients and showed diagnostic value with an ROC AUC of 0.881. Functionally, circFOXP1 overexpression protects H/R-stressed AC16 cells and AMI mice by reducing apoptosis, inflammation, and oxidative stress. The study supports a circFOXP1/miR-9-3p mechanism in AMI-related heart injury. |
| Confidence score: |
0.7126 |