| Expression pattern: |
DN |
| Associated gene: |
CPT1A |
| Associated microRNA: |
miR-124-3p |
| Biological function: |
circHIPK3 promotes CPT1A-mediated fatty acid oxidation activity, endothelial cell proliferation, cell cycle progression, and tube formation; circHIPK3 knockdown suppresses endothelial cell angiogenesis in EOPE. |
| Molecular mechanism: |
circHIPK3 acts as a ceRNA/molecular sponge for miR-124-3p to regulate CPT1A expression, thereby modulating CPT1A-mediated fatty acid oxidation and endothelial angiogenesis. |
| Biological pathway or process: |
lipid metabolism (promotes); proliferation (promotes); cell cycle (promotes); angiogenesis (promotes); ceRNA regulation (promotes) |
| Detected method: |
Q
|
| Validation methods: |
Sanger Sequencing; RT-qPCR; Clinical Sample Validation; Nuclear-Cytoplasmic Fractionation; Luciferase Reporter Assay; Transfection; CCK8; Cell Cycle Assay; Tube Formation Assay; Western Blot; Bioinformatics Analysis |
| Clinical significance: |
Reduced circHIPK3 expression in placental tissues from EOPE patients is associated with endothelial cell dysfunction and aberrant angiogenesis, suggesting the circHIPK3/miR-124-3p/CPT1A axis as a potential therapeutic target. |
| Description: |
In EOPE, circHIPK3 is down-regulated in placental tissues and is mainly localized in the cytoplasm of endothelial cells. The study shows that circHIPK3 acts as a ceRNA for miR-124-3p to maintain CPT1A expression, supporting CPT1A-mediated fatty acid oxidation, endothelial cell proliferation, cell cycle progression, and tube formation. Loss of circHIPK3 impairs endothelial angiogenesis, which may contribute to aberrant angiogenesis in EOPE. |
| Confidence score: |
0.7404 |