| Expression pattern: |
UP |
| Associated gene: |
HIF-1alpha, CDC42BPB, RNA polymerase II (Pol II) |
| Associated microRNA: |
- |
| Biological function: |
circCDC42BPB promotes hypoxia-triggered RA-FLS proliferation, cell cycle progression, migration, and inflammatory response, and its overexpression partially abrogates the inhibitory effects of TMP. |
| Molecular mechanism: |
TMP inhibits HIF-1alpha-induced circCDC42BPB transcription under hypoxic conditions; HIF-1alpha binds the HREs in the CDC42BPB promoter region and increases transcription of the host gene, activating circCDC42BPB. |
| Biological pathway or process: |
HIF-1 signaling (promotes); proliferation (promotes); cell cycle (promotes); migration (promotes); inflammation (promotes) |
| Detected method: |
Q
M
|
| Validation methods: |
RNase R Treatment; RT-qPCR; Microarray; Nuclear-Cytoplasmic Fractionation; Clinical Sample Validation; Luciferase Reporter Assay; ChIP / ChIP-seq; Transfection; CCK8; EdU Staining; Cell Cycle Assay; Wound Healing Assay; Transwell Assay; ELISA; Western Blot; ROC Analysis; Bioinformatics Analysis |
| Clinical significance: |
circCDC42BPB was highly expressed in serum of RA patients and showed diagnostic potential for RA with AUC 0.912. |
| Description: |
hsa_circ_0005178/circCDC42BPB is up-regulated in RA patients and hypoxia-treated RA-FLSs and is reduced by TMP treatment. Functionally, circCDC42BPB promotes hypoxia-induced RA-FLS proliferation, cell cycle progression, migration, and inflammatory responses, counteracting TMP-mediated protection. Mechanistically, HIF-1alpha promotes circCDC42BPB transcription via the CDC42BPB promoter, forming a TMP/HIF-1alpha/circCDC42BPB regulatory axis with potential diagnostic and therapeutic relevance in RA. |
| Confidence score: |
0.8256 |