| Expression pattern: |
UP |
| Associated gene: |
HuR, Cblb, ACSL4 |
| Associated microRNA: |
miR-671-5p |
| Biological function: |
CircBbs9 promotes lung epithelial cell ferroptosis and exacerbates LPS-induced acute lung injury; CircBbs9 knockdown reduces pulmonary pathological injury, alleviates ferroptosis, increases cell viability, and reduces ACSL4 expression. |
| Molecular mechanism: |
CircBbs9 binds HuR to reduce Cblb mRNA stability and inhibit Cblb expression, decreasing Cblb-mediated ubiquitination and degradation of ACSL4; CircBbs9 also acts through a ceRNA mechanism by competitively binding miR-671-5p to upregulate ACSL4 expression. |
| Biological pathway or process: |
ferroptosis (promotes); inflammation (promotes); ubiquitination (inhibits); mRNA stability (inhibits); ceRNA regulation (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RNase R Treatment; Actinomycin D / DRB Stability Assay; RT-qPCR; FISH / smFISH; Nuclear-Cytoplasmic Fractionation; RIP (RNA Immunoprecipitation); RNA Pull-Down; Co-IP; Luciferase Reporter Assay; Transfection; CCK8; Flow Cytometry（Non-apoptosis/cycle）; In Vivo Animal Model; H&E Staining; ELISA; Western Blot; Bioinformatics Analysis |
| Clinical significance: |
- |
| Description: |
CircBbs9 is up-regulated in LPS-induced acute lung injury mouse and lung epithelial cell models. It promotes ferroptosis and inflammatory lung injury by binding HuR to reduce Cblb mRNA stability and ACSL4 ubiquitination/degradation, and by sponging miR-671-5p to increase ACSL4 expression. Knockdown of CircBbs9 alleviates lung tissue injury, reduces ferroptosis markers, and improves lung epithelial cell viability. |
| Confidence score: |
0.7998 |