| Expression pattern: |
UP |
| Associated gene: |
forkhead box A1 (FOXA1), FOXA1 |
| Associated microRNA: |
miR-338 |
| Biological function: |
Aggravates LPS-induced HK2 cell injury; promotes apoptosis, inflammation and oxidative stress; suppresses cell viability and causes G0/G1 arrest. |
| Molecular mechanism: |
ceRNA mechanism: circHIPK3 acts as a molecular sponge for miR-338 to regulate FOXA1 expression. |
| Biological pathway or process: |
apoptosis (promotes); proliferation (inhibits); inflammation (promotes); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Clinical Sample Validation; Luciferase Reporter Assay; RIP (RNA Immunoprecipitation); Nuclear-Cytoplasmic Fractionation; Actinomycin D / DRB Stability Assay; Transfection; CCK8; Annexin V/PI Flow Cytometry; Cell Cycle Assay; ELISA; Western Blot; Bioinformatics Analysis |
| Clinical significance: |
circHIPK3 might be a potential biomarker and therapeutic target for sepsis-induced AKI patients. |
| Description: |
circHIPK3 is up-regulated in serum from septic AKI patients and in LPS-treated HK2 cells. It predominantly localizes to the cytoplasm and aggravates LPS-induced HK2 cell injury by sponging miR-338, thereby relieving miR-338-mediated suppression of FOXA1. circHIPK3 knockdown attenuates apoptosis, inflammation and oxidative stress and improves cell viability, suggesting potential biomarker/therapeutic relevance in sepsis-induced AKI. |
| Confidence score: |
0.7795 |