Basic Information
| LncRNA/CircRNA Name | HAGLROS |
| Synonyms | HAGLROS |
| Region | GRCh38_2:176177717-176179008 |
| Ensemble | ENSG00000226363 |
| Refseq | NR_110457 |
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 | gastric cancer |
| ICD-0-3 | C16 |
| Methods | RNA-seq, Microarray, qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP |
| Sample | GC tissues, gastric cancer cell lines (SGC-7901, BGC-823, HGC-27, MGC-803 and AGS) |
| Expression Pattern | up-regulated |
| Function Description | HAGLROS,whose expression was significantly increased and correlated with outcomes of GC patients Exogenous down-regulation of HAGLROS expression significantly suppressed the cell proliferation,invasion and migration.HAGLROS was a direct target of transcriptional factor STAT3.Moreover,HAGLROS knockdown decreased mTOR expression and increased autophagy-related genes ATG9A and ATG9B expression.Further,HAGLROS regulated mTOR signals in two manners.HAGLROS competitively sponged miR-100-5p to increase mTOR expression by antagonizing miR-100-5p-mediated mTOR mRNA inhibition. |
| Pubmed ID | 29329543 |
| Year | 2018 |
| Title | STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy. |
External Links
| Links for HAGLROS | GenBank HGNC NONCODE |
| Links for gastric cancer | OMIM COSMIC |