Basic Information
| LncRNA/CircRNA Name | SAMMSON |
| Synonyms | NA |
| Region | GRCh38_3:69999550-70518064 |
| Ensemble | ENSG00000240405 |
| Refseq | NR_110000 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | apoptosis | Drug | ||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | glioblastoma |
| ICD-0-3 | NA |
| Methods | qPCR, Western blot etc. |
| Sample | GBM tissues and adjacent normal tissues, cell lines (U87MG, T98G, U251, LN229, and A172) |
| Expression Pattern | up-regulated |
| Function Description | SAMMSON was highly expressed in GBM tissues and cells. SAMMSON knockdown suppressed cell viability and increased LDH release in GBM cells. Moreover, SAMMSON silencing impeded the invasive ability of GBM cells by regulating epithelial-to-mesenchymal transition (EMT). Furthermore, SAMMSON downregulation increased the apoptotic rate and caspase-3 activity in GBM cells. Additionally, it was demonstrated that the PI3K/Akt pathway was inhibited following SAMMSON silencing in GBM cells. |
| Pubmed ID | 32236901 |
| Year | 2020 |
| Title | LncRNA SAMMSON Knockdown Inhibits the Malignancy of Glioblastoma Cells by Inactivation of the PI3K/Akt Pathway |
External Links
| Links for SAMMSON | GenBank HGNC NONCODE |
| Links for glioblastoma | OMIM COSMIC |