| Expression pattern: |
UP |
| Associated gene: |
SLC1A5, Ago2 |
| Associated microRNA: |
miR-515-5p |
| Biological function: |
circAKT3 promotes gastric cancer cell proliferation, survival, glutamine metabolism and tumor growth; circAKT3 knockdown inhibits proliferation, survival, glutamine uptake and in vivo tumor growth and promotes apoptosis. |
| Molecular mechanism: |
circAKT3 acts as a miR-515-5p sponge and relieves miR-515-5p-mediated inhibition of SLC1A5, thereby increasing SLC1A5 expression and promoting malignant behaviors and glutamine metabolism in gastric cancer cells. |
| Biological pathway or process: |
proliferation (promotes); apoptosis (inhibits); glutaminolysis (promotes); ceRNA regulation (promotes) |
| Detected method: |
Q
|
| Validation methods: |
RNase R Treatment; Actinomycin D / DRB Stability Assay; RT-qPCR; Clinical Sample Validation; Transfection; CCK8; EdU Staining; Colony Formation Assay; Annexin V/PI Flow Cytometry; Western Blot; Bioinformatics Analysis; Luciferase Reporter Assay; RIP (RNA Immunoprecipitation); IHC (Immunohistochemistry); In Vivo Animal Model |
| Clinical significance: |
- |
| Description: |
circAKT3 is up-regulated in gastric cancer tissues and cell lines. It functions as an oncogenic circRNA by sponging miR-515-5p to increase SLC1A5 expression, thereby promoting proliferation, survival, glutamine metabolism and tumor growth. Knockdown of circAKT3 suppresses malignant phenotypes and may represent a potential therapeutic strategy. |
| Confidence score: |
0.8298 |