Basic Information
| LncRNA/CircRNA Name | HAGLROS |
| Synonyms | NA |
| Region | GRCh38_2:176177717-176179008 |
| Ensemble | ENSG00000226363 |
| Refseq | NR_110457 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | autophagy/apoptosis | Drug | ||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | hepatocellular carcinoma |
| ICD-0-3 | C22.0 |
| Methods | qPCR , Luciferase reporter assay , Western blot , RIP etc. |
| Sample | HCC tissues and matched nontumor tissues ,normal liver cell line HL-7702 and hepatoma cell lines(SK-Hep1,MHCC97L, MHCC97H, Huh7, and HepG2.2.15) |
| Expression Pattern | up-regulated |
| Function Description | The level of HAGLROS was higher in HCC tissues and correlated with clinical performances including tumor stages or tumor differentiation.In contrast to the lower level, a higher level of HAGLROS correlated with a shorter survival time of patients with HCC. The suppression of HAGLROS decreased cell viability, promoted apoptosis, and inhibited autophagy.Moreover, HAGLROS negatively regulated miR-5095 expression, which further regulated HCC cell viability, apoptosis, and autophagy.ATG12 was targeted by miR-5095 and was then involved in miR-5095-regulated HCC cell biological processes including viability, apoptosis, and autophagy. Furthermore, overexpression of HAGLROS activated PI3K/AKT/mTOR signals. |
| Pubmed ID | 31082725 |
| Year | 2019 |
| Title | Long Noncoding RNA HAGLROS Promotes Cell Proliferation, Inhibits Apoptosis and Enhances Autophagy via Regulating miR-5095/ATG12 Axis in Hepatocellular Carcinoma Cells |
External Links
| Links for HAGLROS | GenBank HGNC NONCODE |
| Links for hepatocellular carcinoma | OMIM COSMIC |