Basic Information
| LncRNA/CircRNA Name | HAGLR |
| Synonyms | HOXD-AS1 |
| Region | GRCh38_2:176164051-176188958 |
| Ensemble | ENSG00000224189 |
| Refseq | NR_033979 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | apoptosis | Drug | ||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | lung adenocarcinoma |
| ICD-0-3 | C34 |
| Methods | Microarray, qPCR , in vitro knockdown , Western blot , RIP etc. |
| Sample | primary lung cancer tissues and adjacent normal tissues ,lung cancer cell lines (A549, SPC-A1, NCI-H1299, NCI-H460,NCI-H520 and HCC827) and a normal human bronchial epithelial cell line (HBE) |
| Expression Pattern | down-regulated |
| Function Description | Here, we reported that HAGLR (also called HOXD-AS1) was frequently down-regulated in lung adenocarcinoma (LUAD) tissues, and decreased HAGLR expression was clinically associated with shorter survival of LUAD patients.HAGLR could attenuate LUAD cell growth in vitro and in vivo. Mechanistically, HAGLR could physically interact with DNMT1, and recruit DNMT1 on E2F1 promoter to increase local DNA methylation.Overall, our study demonstrated that HAGLR promoted LUAD progression by recruiting DNMT1 to modulate the promoter methylation and expression of E2F1, which expanded potential therapeutic strategies for LUAD treatment. |
| Pubmed ID | 31194977 |
| Year | 2019 |
| Title | Long Non-Coding RNA-HAGLR Suppressed Tumor Growth of Lung Adenocarcinoma Through Epigenetically Silencing E2F1 |
External Links
| Links for HAGLR | GenBank HGNC NONCODE |
| Links for lung adenocarcinoma | OMIM COSMIC |