Basic Information
| LncRNA/CircRNA Name | TP73-AS1 |
| Synonyms | NA |
| Region | NA |
| Ensemble | ENSG00000227372 |
| Refseq | NR_033708 |
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 | qPCR, Western blot, in vitro knockdown, etc. |
| Sample | LAD tissues, Normal human bronchial epithelial cells (BEAS-2B) and LAD cell lines (H157, A549, H1299, H1975 and HCC827) |
| Expression Pattern | up-regulated |
| Function Description | TP73-AS1 expression was markedly increased in LAD tissues and cell lines and its overexpression was strongly associated with poor clinical outcomes. Then the loss/gain-of-function assays elucidated that TP73-AS1 contributed to cell proliferation, migration and invasion in vitro, and the in vivo experiments illustrated that its knockdown inhibited tumor growth and metastasis. What s more, we discovered that PI3K/AKT pathway was activated both in LAD tissues and cell lines but inactivated under TP73- AS1 silence. Moreover, the activation of this pathway could rescue the inhibitory effects of TP73-AS1 suppression on LAD cellular processes in partial. These data suggested that TP73-AS1 served as an oncogene in LAD partially through activating PI3K/AKT pathway and it could be a potential target for diagnosis and treatment of LAD. |
| Pubmed ID | 30541897 |
| Year | 2018 |
| Title | LncRNA TP73-AS1 promoted the progression of lung adenocarcinoma via PI3K/AKT pathway |
External Links
| Links for TP73-AS1 | GenBank HGNC NONCODE |
| Links for Lung adenocarcinoma | OMIM COSMIC |