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 | apoptosis | Drug | temozolomide | |
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | glioma |
| ICD-0-3 | NA |
| Methods | qPCR, Luciferase reporter assay, other |
| Sample | glioma cell lines (U251 and LN229) |
| Expression Pattern | up-regulated |
| Function Description | Knockdown of H19 in U251TMZ and LN229TMZ cells decreased half maximal inhibitory concentration (IC50) values for TMZ and increased cell apoptosis, and H19 overexpression in U251 and LN229 cells led to the opposite effects, indicating that the H19 confers TMZ resistance to glioma cells. Furthermore, knockdown of H19 decreased the NF-?B signaling, which was revealed by repressed reporter activity and declined expression of its downstream targets in TMZ-resistant glioma cells. In contrast, H19 overexpression in U251 and LN229 cells resulted in an increase in NF-?B activation. Blockage of NF-?B activation by its inhibitor abolished TMZ resistance caused by H19 overexpression. Addition of H2O2 to induce oxidative stress largely reversed TMZ sensitivity caused by H19 knockdown. |
| Pubmed ID | 30323617 |
| Year | 2018 |
| Title | H19 Induced by Oxidative Stress Confers Temozolomide Resistance in Human Glioma Cells via Activating NF-?B Signaling |
External Links
| Links for H19 | GenBank HGNC NONCODE |
| Links for glioma | OMIM COSMIC |