| Expression pattern: |
UP |
| Associated gene: |
TFII-I, HNRNPL, EIF3I, EIF2S1, FTO, FOS |
| Associated microRNA: |
- |
| Biological function: |
promotes tumor cell growth, proliferation, colony formation, migration, invasion, and metastasis |
| Molecular mechanism: |
circARHGAP35 is translated (m6A-dependent) into a truncated oncogenic protein that interacts with TFII-I in the nucleus; HNRNPL promotes circARHGAP35 biogenesis |
| Biological pathway or process: |
proliferation (promotes); migration (promotes); invasion (promotes); metastasis (promotes); m6A modification (promotes); other pathway/process (other) |
| Detected method: |
Q
B
S
|
| Validation methods: |
RNA-seq; RT-qPCR; Back-Splice Junction PCR / divergent primers PCR; Sanger Sequencing; RNase R Treatment; Actinomycin D / DRB Stability Assay; FISH / smFISH; Nuclear-Cytoplasmic Fractionation; Northern Blot; Clinical Sample Validation; Cohort Study; Survival Analysis; Transfection; CCK8; Colony Formation Assay; Transwell Assay; In Vivo Animal Model; H&E Staining; RIP (RNA Immunoprecipitation); Luciferase Reporter Assay; Co-IP; Western Blot; MeRIP / MeRIP-seq; RNA Pull-Down |
| Clinical significance: |
High abundance of circARHGAP35 is associated with shorter overall survival (OS), shorter disease free survival (DFS), and a higher recurrence rate in HCC patients. |
| Description: |
circARHGAP35 (from ARHGAP35 exon2-exon3 back-splicing) is up-regulated in HCC and CRC and promotes proliferation, migration, invasion, and metastasis. It is m6A-dependently translated into a truncated oncogenic protein that interacts with TFII-I in the nucleus, and its biogenesis is promoted by the RBP HNRNPL; high circARHGAP35 predicts worse survival in HCC patients. |
| Confidence score: |
0.892 |