Basic Information
| LncRNA/CircRNA Name | T-ALL-R-lncR1 |
| Synonyms | NA |
| Region | NA |
| Ensemble | NA |
| Refseq | NA |
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 | acute lymphoblastic leukemia |
| ICD-0-3 | NA |
| Methods | qPCR, RNAi, Western blot etc. |
| Sample | T-ALL jurkat cell |
| Expression Pattern | up-regulated |
| Function Description | T-ALL-R-LncR1 was not observed in human normal tissues. However, an obvious expression was observed in some tumor tissues. T-ALL-R-LncR1 was markedly expressed in neoplastic T lymphocytes of 11 cases out of 21 children with T-ALL, indicating that T-ALL-R-LncR1 might be associated with T-ALL. T-ALL-R-LncR1 knockdown predisposed Jurkat cells to undergo pro-apoptotic factor Par-4-induced apoptosis. Further studies revealed that T-ALL-R-LncR1 knockdown facilitated the formation of a Par-4/THAP1 protein complex, resulting in the activation of caspase-3 and an increase of pro-apoptotic Smac protein in T-ALL cells |
| Pubmed ID | 23906015 |
| Year | 2014 |
| Title | A novel long non-coding RNA T-ALL-R-LncR1 knockdown and Par-4 cooperate to induce cellular apoptosis in T-cell acute lymphoblastic leukemia cells |
External Links
| Links for T-ALL-R-lncR1 | GenBank HGNC NONCODE |
| Links for acute lymphoblastic leukemia | OMIM COSMIC |