| Expression pattern: |
DN |
| Associated gene: |
GSK-3beta, beta-catenin, Ago2 |
| Associated microRNA: |
miR-624-5p |
| Biological function: |
inhibits proliferation, migration, invasion, and tumor growth in HCC |
| Molecular mechanism: |
Acts as a miRNA sponge for miR-624-5p to upregulate GSK-3beta, facilitating beta-catenin degradation and preventing its nuclear translocation, thereby inactivating GSK-3beta/beta-catenin (Wnt/beta-catenin) signaling. |
| Biological pathway or process: |
proliferation (inhibits); migration (inhibits); invasion (inhibits); Wnt/beta-catenin (inhibits); ceRNA regulation (promotes) |
| Detected method: |
Q
S
|
| Validation methods: |
RNA-seq; Bioinformatics Analysis; RT-qPCR; Back-Splice Junction PCR / divergent primers PCR; RNase R Treatment; Sanger Sequencing; Actinomycin D / DRB Stability Assay; FISH / smFISH; RIP (RNA Immunoprecipitation); RNA Pull-Down; Luciferase Reporter Assay; Transfection; CCK8; Colony Formation Assay; Transwell Assay; Western Blot; IHC (Immunohistochemistry); In Vivo Animal Model; H&E Staining; Survival Analysis; Clinical Sample Validation; Cohort Study |
| Clinical significance: |
Higher levels of circLIFR in HCC patients correlated with favorable overall survival and recurrence-free survival; higher expression was correlated with lower AFP, earlier BCLC stage, earlier TNM stage, smaller tumor size, and non-microvascular invasion. |
| Description: |
circLIFR (hsa_circ_0072309), derived from LIFR, is down-regulated in HCC tissues and functions as a tumor suppressor. It sponges miR-624-5p to increase GSK-3beta, promoting beta-catenin degradation and inhibiting Wnt/beta-catenin signaling, thereby reducing HCC cell proliferation and invasion and suppressing tumor growth in xenograft models. Higher circLIFR levels are associated with better OS and RFS in the patient cohort. |
| Confidence score: |
0.896 |