Basic Information
| LncRNA/CircRNA Name | MALAT1 |
| Synonyms | MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 |
| Region | GRCh38_11:65497688-65506516 |
| Ensemble | ENSG00000251562 |
| Refseq | NR_002819 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | Drug | |||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | glioma |
| ICD-0-3 | NA |
| Methods | qPCR, Western blot, RIP, ChIP, Luciferase reporter assay etc. |
| Sample | glioma tissues, cell lines (hCMEC/D3, ECs) |
| Expression Pattern | up-regulated |
| Function Description | Our results proved that MALAT1 expression was up-regulated in brain microvessels of human glioma and glioma endothelial cells (GECs) which were obtained by co-culturing endothelial cells with glioma cells. Functionally, knockdown of MALAT1 resulted in an impairment and increased the permeability of BTB as well as decreased the expression of ZO-1, occludin and claudin-5 in GECs. Further, there was reciprocal repression between MALAT1 and miR-140, and miR-140 mediated the effects that MALAT1 knockdown exerted. Mechanistic investigations defined that nuclear factor YA (NFYA), a CCAAT box-binding transcription factor, was a direct and functional downstream target of miR-140, which was involved in the MALAT1 knockdown induced regulation of BTB function. |
| Pubmed ID | 26619802 |
| Year | 2015 |
| Title | Knockdown of long non-coding RNA MALAT1 increases the blood-tumor barrier permeability by up-regulating miR-140 |
External Links
| Links for MALAT1 | GenBank HGNC NONCODE |
| Links for glioma | OMIM COSMIC |