Basic Information
| LncRNA/CircRNA Name | SPRY4-IT1 |
| Synonyms | NA |
| Region | NA |
| Ensemble | ENSG00000281881 |
| Refseq | NR_131221 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | apoptosis | Drug | ||
| Variant | Cell Growth | Circulating | 2 | ||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | gastric cancer |
| ICD-0-3 | C16 |
| Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP |
| Sample | The normal gastric mucosa epithelial GES-1 cell line and three different differentiated GC cell lines, MKN28, SGC7901, and BGC823, GC tissues and paired adjacent noncancerous tissues |
| Expression Pattern | up-regulated |
| Function Description | SPRY4-IT1 was upregulated in GC. In vitro experiments revealed that SPRY4-IT1 knockdown significantly inhibited GC cell proliferation by causing G1 arrest and promoting apoptosis, whereas SPRY4-IT1 overexpression promoted cell growth. Further functional assays indicated that SPRY4-IT1 overexpression significantly promoted cell migration and invasion. Bioinformatics analysis predicted that there is a SPRY4-IT1/miR-101-3p/AMPK axis in GC progression. A dual-luciferase reporter system validated the direct interaction of SPRY4-IT1, miR-101-3p, and AMPK. Western blot verified that the inhibition of SPRY4- IT1 decreased AMPK expression. Furthermore, silencing SPRY4-IT1 suppressed GC growth in vivo. Importantly, we demonstrated that SPRY4-IT1 was upregulated in serum exosomes from GC patients and correlated with cancer metastasis. |
| Pubmed ID | 31330497 |
| Year | 2019 |
| Title | lncRNA SPRY4-IT1 Regulates Cell Proliferation and Migration by Sponging miR-101-3p and Regulating AMPK Expression in Gastric Cancer |
External Links
| Links for SPRY4-IT1 | GenBank HGNC NONCODE |
| Links for gastric cancer | OMIM COSMIC |