Basic Information
| LncRNA/CircRNA Name | AGAP2-AS1 |
| Synonyms | NA |
| Region | GRCh38_12:57726271-57728356 |
| Ensemble | ENSG00000255737 |
| Refseq | NR_027032 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | apoptosis | Drug | ||
| Variant | Cell Growth | Circulating | 2 | ||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | glioblastoma |
| ICD-0-3 | NA |
| Methods | qRT-PCR , Western blot , RIP etc. |
| Sample | GBM tumor tissues and matched non-cancerous tissues,GBM cell lines (A172, U87/MG, U251/MG, LN229, and SHG44) ,normal human astrocytes (NHA) |
| Expression Pattern | up-regulated |
| Function Description | AGAP2-AS1 expression was up-regulated in GBM tissues and cells. High AGAP2-AS1 expression may predict a poor prognosis in GBM patients. Functionally, silencing of AGAP2-AS1 suppressed proliferation and invasion, while enhanced apoptosis in GBM cells. Overexpression of AGAP2-AS1 promoted cell proliferation and invasion. Mechanically, AGAP2-AS1 could interact with EZH2 and LSD1, recruiting them to TFPI2 promoter region to inhibit its transcription.Also, suppression of AGAP2-AS1 impaired tumor growth of GBM in vivo.In summary, AGAP2-AS1 exerts oncogenic functions in GBM by epigenetically silencing TFPI2 expression through binding to EZH2 and LSD1 |
| Pubmed ID | 31186379 |
| Year | 2019 |
| Title | Long Non-Coding RNA AGAP2-AS1 Exerts Oncogenic Properties in Glioblastoma by Epigenetically Silencing TFPI2 Through EZH2 and LSD1 |
External Links
| Links for AGAP2-AS1 | GenBank HGNC NONCODE |
| Links for glioblastoma | OMIM COSMIC |