| Expression pattern: |
UP |
| Associated gene: |
- |
| Associated microRNA: |
- |
| Biological function: |
Promotes gastric cancer cell proliferation, migration, invasion and epithelial-mesenchymal transition; high expression is associated with tumor size, vascular invasion, lymph node metastasis, AJCC stage and poor prognosis. |
| Molecular mechanism: |
circPCSK5 promotes EMT phenotype conversion in gastric cancer cells, with decreased E-cadherin and increased N-cadherin and Vimentin upon overexpression; the precise upstream molecular mechanism was not determined. |
| Biological pathway or process: |
proliferation (promotes); migration (promotes); invasion (promotes); EMT (promotes) |
| Detected method: |
Q
S
|
| Validation methods: |
Sanger Sequencing; RNase R Treatment; Actinomycin D / DRB Stability Assay; RT-qPCR; FISH / smFISH; Nuclear-Cytoplasmic Fractionation; Clinical Sample Validation; Transfection; CCK8; EdU Staining; Transwell Assay; Western Blot; Cohort Study; Survival Analysis; Bioinformatics Analysis |
| Clinical significance: |
High circPCSK5 expression is associated with tumor size, vascular invasion, lymph node metastasis, AJCC stage, shorter overall survival and disease-free survival, and is an independent risk factor for poor prognosis in gastric cancer patients. |
| Description: |
circPCSK5 (hsa_circ_0087234), derived from PCSK5, is up-regulated in gastric cancer tissues and cell lines. Its high expression predicts poorer overall and disease-free survival, while functional assays show that circPCSK5 promotes gastric cancer cell proliferation, migration, invasion and EMT. |
| Confidence score: |
0.8218 |