| Expression pattern: |
UP |
| Associated gene: |
KRAS, Ago2 |
| Associated microRNA: |
miR-30b |
| Biological function: |
promotes proliferation, invasion and migration; promotes metastasis; induces cetuximab resistance; inhibits cetuximab-induced apoptosis |
| Molecular mechanism: |
circIFNGR2 acts as a ceRNA sponging miR-30b, indirectly upregulating KRAS and activating downstream signaling (p-ERK, p-AKT), leading to cetuximab resistance |
| Biological pathway or process: |
proliferation (promotes); migration (promotes); invasion (promotes); metastasis (promotes); apoptosis (inhibits); ERK (promotes); PI3K/AKT (promotes); drug resistance (promotes); ceRNA regulation (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RT-qPCR; Sanger Sequencing; FISH / smFISH; RNA Pull-Down; RIP (RNA Immunoprecipitation); Luciferase Reporter Assay; Transfection; CCK8; Colony Formation Assay; Transwell Assay; Wound Healing Assay; Annexin V/PI Flow Cytometry; Western Blot; IHC (Immunohistochemistry); In Vivo Animal Model; H&E Staining; Clinical Sample Validation; Survival Analysis; Bioinformatics Analysis |
| Clinical significance: |
circIFNGR2 upregulation was significantly correlated with the tumor TNM stage of CRC; high expression of circIFNGR2 tightly related to a poor prognosis; potential chemotherapy resistance marker/diagnostic biomarker in CRC |
| Description: |
circIFNGR2 is up-regulated in colorectal cancer tissues and promotes CRC cell proliferation, invasion/migration, metastasis, and in vivo tumor growth. Mechanistically, it localizes to the cytoplasm and sponges miR-30b, thereby relieving miR-30b-mediated repression of KRAS and enhancing downstream ERK/AKT signaling, which contributes to cetuximab resistance (especially in WT-KRAS CRC). High circIFNGR2 expression is associated with advanced stage and poor prognosis. |
| Confidence score: |
0.849 |