Basic Information
| LncRNA/CircRNA Name | LINC00665 |
| Synonyms | NA |
| Region | GRCh38_19:36313067-36331718 |
| Ensemble | ENSG00000232677 |
| Refseq | NR_038278 |
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 | lung adenocarcinoma |
| ICD-0-3 | C34 |
| Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, etc. |
| Sample | LUAD tissues, NSCLC cell lines (A549, H1299, H1650, H520, SPCA-1, and SK-MES-1), human bronchial epithelial cell (16HBE) and HEK-293T |
| Expression Pattern | up-regulated |
| Function Description | linc00665 (ENST00000590622), which was markedly upregulated in lung adenocarcinoma (LUAD) tissues and might serve as an independent predictor for poor prognosis. Functional assays indicated that linc00665 reinforced LUAD cell proliferation and metastasis in vitro and in vivo. Mechanistically, transcription factor SP1 induced the transcription of linc00665 in LUAD cells, which exerted its oncogenic role by functioning as competing endogenous RNA (ceRNA) for miR-98 and subsequently activating downstream AKR1B10-ERK signaling pathway. Together, our study elucidates oncogenic roles of linc00665 miR98 AKR1B10 axis in LUAD tumorigenesis, which may serve as potential diagnostic biomarkers and therapeutic targets. |
| Pubmed ID | 30692511 |
| Year | 2019 |
| Title | Long non-coding RNA linc00665 promotes lung adenocarcinoma progression and functions as ceRNA to regulate AKR1B10-ERK signaling by sponging miR-98. |
External Links
| Links for LINC00665 | GenBank HGNC NONCODE |
| Links for lung adenocarcinoma | OMIM COSMIC |