| Expression pattern: |
UP |
| Associated gene: |
JNK/p38 pathways, NF-kappaB pathways |
| Associated microRNA: |
miR-181a, miR-181a-5p |
| Biological function: |
circZNF652 promoted LPS-induced inflammatory damage, apoptosis, Cox-2 expression and inflammatory factor production in WI-38 cells; knockdown of circZNF652 increased cell viability and reduced apoptosis and inflammation. |
| Molecular mechanism: |
circZNF652 negatively regulated miR-181a, and circZNF652 knockdown remitted LPS-induced inflammatory damage through deactivation of NF-kappaB and JNK/p38 pathways by up-regulating miR-181a. |
| Biological pathway or process: |
NF-kappaB (promotes); MAPK (promotes); apoptosis (promotes); inflammation (promotes); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Transfection; CCK8; Annexin V/PI Flow Cytometry; Western Blot; ELISA; Bioinformatics Analysis |
| Clinical significance: |
This basic research on circZNF652 provides new directions for clinical treatment of IP. |
| Description: |
circZNF652 was up-regulated in the LPS-induced WI-38 cell inflammatory injury model of infantile pneumonia. Silencing circZNF652 alleviated inflammatory injury by increasing cell viability and reducing apoptosis, Cox-2, and inflammatory cytokines. Mechanistically, circZNF652 negatively regulated miR-181a and promoted activation of the NF-kappaB and JNK/p38 pathways. |
| Confidence score: |
0.4611 |