Basic Information
| LncRNA/CircRNA Name | CUDR |
| Synonyms | UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 |
| Region | GRCh38_19:15828206-15836326 |
| Ensemble | ENSG00000214049 |
| Refseq | NR_015379 |
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 | pancreatic ductal adenocarcinoma |
| ICD-0-3 | C25.3 |
| Methods | qPCR, Western blot, Microarray, other |
| Sample | PDAC tissues and cell lines (Panc-1, CFPAC-1, Capan-1, Aspc-1, SW1990, BxPC-3,Miapaca-2 and HPAC) |
| Expression Pattern | up-regulated |
| Function Description | In the present study, a microarray assay was used to screen for differently expressed lncRNAs in PDAC and it was identified that cancer upregulated drug resistance (CUDR) was upregulated in PDAC. CUDR increased PDAC cell proliferation, migration and invasion, inhibited apoptosis, and promoted drug resistance; it also regulated the PDAC cell epithelial-mesenchymal transition. The CUDR-induced PDAC malignant phenotypes is via the protein kinase B and extracellular-signal-regulated kinase signaling pathways. Downregulation of CUDR may be a novel therapeutic strategy to prevent PDAC development and drug resistance in the future. |
| Pubmed ID | 30272271 |
| Year | 2018 |
| Title | Long Non-Coding RNA CUDR Promotes Malignant Phenotypes in Pancreatic Ductal Adenocarcinoma via Activating AKT and ERK Signaling Pathways |
External Links
| Links for CUDR | GenBank HGNC NONCODE |
| Links for pancreatic ductal adenocarcinoma | OMIM COSMIC |