| Detected method: |
Q
|
| Detected method confidence |
High
|
| Expression pattern: |
|
| Associated gene: |
- |
| Associated microRNA: |
hsa-miR-217 |
| Biological function: |
hsa_circ_0004543 expressions were compared between 40 paired paracancerous and cancerous specimens from CC patients and between 6 CC cell lines and a normal human cervical epithelial cell line based on qRT-PCR. Potential complementary binding sites between hsa-miR-217 and hsa_circ_0004543 were predicted using the interactome, while binding sites for the hypoxia-inducible factor-1a (HIF-1a) were predicted by TargetScan. The function and mechanism of hsa_circ_0004543 in the development of CC were estimated by silencing hsa_circ_0004543 with/without hsa-miR-217 or HIF-1a overexpression. The association between gene expressions was evaluated with Pearsons correlation analysis. |
| Molecular mechanism: |
Molecular mechanisms were explored by ribonucleic acid (RNA) pulldown, dual-luciferase activity, and rescue experimental assays. Our results revealed that the hsa_circ_0004543 expression was considerably increased in CC tissues and cells. Its silencing repressed proliferation and metastasis, while it increased apoptosis of CC cells. The investigation of the mechanism showed that hsa-miR-217 silencing or HIF-1a overexpression rescued hsa_circ_0004543, and silencing inhibited malignant phenotypes of CC cells. hsa_circ_0004543 upregulated the HIF-1alpha_xpression by sponging hsa-miR-217 in CC development. |
| Survival: |
- |
Supported
No.: |
1 |
| Description: |
targeting the hsa_circ_0004543/hsa-miR-217/HIF-1alpha_xis might be a potential treatment approach for CC. |