| Expression pattern: |
DN |
| Associated gene: |
EGFR |
| Associated microRNA: |
miR-7 |
| Biological function: |
CDR1as promotes HCC cell proliferation, enhances cell adhesion, promotes G1/S phase transition, and reduces migration; its effect on cell invasion was reported as unaffected in CDR1as-overexpressing HepG2 cells. |
| Molecular mechanism: |
CDR1as regulates HCC cell proliferation and cell cycle at least partly through the miR-7/EGFR axis; quantitative proteomics identified CDR1as-regulated proteins enriched in proliferation and cell-cycle processes. |
| Biological pathway or process: |
proliferation (promotes); cell cycle (promotes); migration (inhibits); EGFR (promotes); ceRNA regulation (other); PI3K/AKT (other); PI3K/AKT/mTOR (other) |
| Detected method: |
Q
H
|
| Validation methods: |
Back-Splice Junction PCR / divergent primers PCR; RT-qPCR; FISH / smFISH; Clinical Sample Validation; Transfection; CCK8; Cell Cycle Assay; Wound Healing Assay; Transwell Assay; Western Blot; IF (Immunofluorescence); Bioinformatics Analysis |
| Clinical significance: |
CDR1as was significantly lower in human HCC tissues than adjacent liver tissues, suggesting disease-associated expression alteration; no diagnostic, prognostic, or survival performance was evaluated in this study. |
| Description: |
This study reports that CDR1as is downregulated in HCC tissues and cell lines, but gain-of-function experiments show that CDR1as promotes HCC cell proliferation, cell-cycle progression, and adhesion while reducing migration. Mechanistically, CDR1as suppresses miR-7 and increases EGFR expression, forming a CDR1as/miR-7/EGFR regulatory axis that contributes to proliferation and cell-cycle effects in HCC cells. |
| Confidence score: |
0.6835 |