Basic Information
| LncRNA/CircRNA Name | CCSlnc362 |
| Synonyms | RP11-362K14.5 |
| Region | NA |
| Ensemble | NA |
| Refseq | NA |
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 | colorectal cancer |
| ICD-0-3 | C19.9 |
| Methods | qPCR, Western blot, Luciferase reporter assay, etc. |
| Sample | CRC tissues, human colorectal epithelial cell line (FHC) and CRC cell lines HCT116, DLD-1, SW480, LOVO, HT29, and RKO,SW1116 and SW620 cells |
| Expression Pattern | up-regulated |
| Function Description | lncRNA CCSlnc362 expression was significantly increased in CRC samples. Follow-up functional experiments elucidated that downregulation of CCSlnc362 inhibited cell proliferation, arrested cell cycle, and promoted apoptosis in CRC cells. The T>C variant of rs1317082 at CCSlnc362 exon 1 created a binding site for miR-4658 to reduce the expression of CCSlnc362 and thus decreased the susceptibility to CRC. Our findings have provided supporting evidence for the protective role of rs1317082 variation and the potential oncogenic role of lncRNA CCSlnc362 in CRC. |
| Pubmed ID | 30518759 |
| Year | 2018 |
| Title | Variant of SNP rs1317082 at CCSlnc362 (RP11-362K14.5) creates a binding site for miR-4658 and diminishes the susceptibility to CRC |
External Links
| Links for CCSlnc362 | GenBank HGNC NONCODE |
| Links for colorectal cancer | OMIM COSMIC |