Basic Information
| LncRNA/CircRNA Name | TUG1 |
| Synonyms | TUG1, LINC00080, NCRNA00080, TI-227H |
| Region | GRCh38_22:30969245-30979395 |
| Ensemble | ENSG00000253352 |
| Refseq | NR_002323 |
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 | intrahepatic cholangiocarcinoma |
| ICD-0-3 | C22 |
| Methods | qPCR, Western blot, Luciferase reporter assay etc. |
| Sample | cell lines (HuH28, HuCCT1, RBE, HCCC-9810) |
| Expression Pattern | up-regulated |
| Function Description | In this study, we investigated the role of TUG1 in the pathogenesis of intrahepatic cholangiocarcinoma (ICC).TUG1 is upregulated in ICC samples, which correlates with poor prognosis and adverse clinical pathological characteristics. Knockdown of TUG1 inhibited the proliferation, motility, and invasiveness of cultured ICC cells, and decreased tumor burden in a xenograft mouse model. When we explored the mechanisms underlying these effects, we found that TUG1 acts as an endogenous competing RNA (ceRNA) that ??ponges??miR-145, thereby preventing the degradation of Sirt3 mRNA and increasing expression of Sirt3 and GDH proteins. Accordingly, glutamine consumption, a-KG production, and ATP levels were dramatically decreased by TUG1 knockdown in ICC cells, and this effect was reversed by miR-145 inhibition. These findings indicate that the TUG1/miR-145/Sirt3/GDH regulatory network may provide a novel therapeutic strategy for treatment of ICC. |
| Pubmed ID | 29371936 |
| Year | 2017 |
| Title | LncRNA TUG1 sponges miR-145 to promote cancer progression and regulate glutamine metabolism via Sirt3/GDH axis |
External Links
| Links for TUG1 | GenBank HGNC NONCODE |
| Links for intrahepatic cholangiocarcinoma | OMIM COSMIC |