Basic Information
| LncRNA/CircRNA Name | circCDR1as |
| Synonyms | circCDR1T, circciRS_7 |
| Region | |
| Ensemble | |
| Refseq |
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 | non small cell lung cancer |
| ICD-0-3 | C34 |
| Methods | qPCR, western blot, other |
| Sample | lung cancer tissues and cell lines (A549 and H460) |
| Expression Pattern | up-regulated |
| Function Description | Patients with high expression of CDR1as had high TNM stage (P=0.004), more lymph nodes metastasis (LNM) (P=0.021) and shorted overall survival time (OS) (P=0.0135). The CDR1as level was an independent prognostic factor for the patients with NSCLC. Overexpression of CDR1as induced increased cell vitalities and growth, which could be abrogated by knockdown of CDR1as or overexpressed miR-7 to induce apoptosis and G1/S arrest. Mechanistically, CDR1as functioned as miR-7 sponges to up-regulate the key target genes of miR-7 including EGFR, CCNE1 and PIK3CD. The results in vivo further confirmed that CDR1as functioned as oncogene to inhibit the anti-tumor effects of tumor suppressor miR-7 by up-regulation of proliferation index Ki-67, EGFR, CCNE1 and PIK3CD levels. |
| Pubmed ID | 30022841 |
| Year | 2018 |
| Title | Overexpressed CDR1as Functions as an Oncogene to Promote the Tumor Progression via miR-7 in Non-Small-Cell Lung Cancer |
External Links
| Links for circCDR1as | GenBank HGNC NONCODE |
| Links for non small cell lung cancer | OMIM COSMIC |