Basic Information
| LncRNA/CircRNA Name | DUSP |
| Synonyms | NA |
| Region | NA |
| Ensemble | NA |
| Refseq | NA |
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 | colon cancer |
| ICD-0-3 | C18 |
| Methods | RNA-seq, qPCR, RNAi etc. |
| Sample | cell lines (V481 and V70) |
| Expression Pattern | down-regulated |
| Function Description | Validation in an independent cohort of normal colon and patient-derived colon cancer cell lines identified a novel lncRNA, lincDUSP, as a potential candidate oncogene. Knockdown of lincDUSP in patient-derived colon tumor cell lines resulted in significantly decreased cell proliferation and clonogenic potential, and increased susceptibility to apoptosis. The knockdown of lincDUSP affects the expression of ~800 genes, and NCI pathway analysis showed enrichment of DNA damage response and cell cycle control pathways. Further, identification of lincDUSP chromatin occupancy sites by ChIRP-Seq demonstrated association with genes involved in the replication-associated DNA damage response and cell cycle control. Consistent with these findings, lincDUSP knockdown in colon tumor cell lines increased both the accumulation of cells in early S-phase and ?H2AX foci formation, indicating increased DNA damage response induction. Taken together, these results demonstrate a key role of lincDUSP in the regulation of important pathways in colon cancer. |
| Pubmed ID | 29743621 |
| Year | 2018 |
| Title | Colon Cancer-Upregulated Long Non-Coding RNA lincDUSP Regulates Cell Cycle Genes and Potentiates Resistance to Apoptosis. |
External Links
| Links for DUSP | GenBank HGNC NONCODE |
| Links for colon cancer | OMIM COSMIC |