Basic Information
| LncRNA/CircRNA Name | H19 |
| Synonyms | H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 |
| Region | GRCh38_11:1995176-2001470 |
| Ensemble | ENSG00000130600 |
| Refseq | NR_002196 |
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 | retinoblastoma |
| ICD-0-3 | C69.2 |
| Methods | Western blot, qPCR, in vitro knockdown RIP etc. |
| Sample | cell lines (WERI-Rb-1, SO-RB50, and Y7, ARPE-19), retinoblastoma tissues |
| Expression Pattern | down-regulated |
| Function Description | H19 is downregulated in retinoblastoma tissues and cell lines. Mechanistically, we identified seven miR-17-92 cluster binding sites on H19, and found that H19 directly bound to miR-17-92 cluster via these seven binding sites. Through binding to miR-17-92 cluster, H19 relieves the suppressing roles of miR-17-92 cluster on p21. Furthermore, H19 represses STAT3 activation induced by miR-17-92 cluster. Hence, our results revealed that H19 upregulates p21 expression,inhibits STAT3 phosphorylation, and downregulates the expression of STAT3 target genes BCL2, BCL2L1, and BIRC5. In conclusion, our data suggested that H19 inhibits retinoblastoma progression via counteracting the roles of miR-17-92 cluster, and implied that enhancing the action of H19 may be a promising therapeutic strategy for retinoblastoma. |
| Pubmed ID | 29143996 |
| Year | 2017 |
| Title | Long non-coding RNA H19 suppresses retinoblastoma progression via counteracting miR-17-92 cluster. |
External Links
| Links for H19 | GenBank HGNC NONCODE |
| Links for retinoblastoma | OMIM COSMIC |