Basic Information
| LncRNA/CircRNA Name | HOTTIP |
| Synonyms | HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 |
| Region | GRCh38_7:27198575-27207259 |
| Ensemble | ENSG00000243766 |
| Refseq | NR_037843 |
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 | renal cell carcinoma |
| ICD-0-3 | C64.9 |
| Methods | qPCR, Western blot, Luciferase reporter assay, other |
| Sample | RCC tissues and cell lines (A-498,786-O, Caki-1, Caki-2 and ACHN) |
| Expression Pattern | up-regulated |
| Function Description | Mechanistic analyses revealed that HOTTIP functioned as a competing endogenous RNA (ceRNA) for hsa-miR-615-3p, and led to the derepression of its endogenous target, insulin-like growth factor-2 (IGF-2), which is a protein hormone that exerts a stimulatory effect on tumor cell growth. miR-615 inhibition reversed the suppressive effects of HOTTIP knockdown on RCC cell progression. HOTTIP regulated IGF-2 expression in a miR-615-dependent manner in RCC cells. In addition, IGF-2 expression was significantly upregulated in the RCC specimens and a positive association between the expression of HOTTIP and IGF-2 in RCC tissues was detected. The effect of HOTTIP was abolished by the siRNA-mediated silencing of IGF-2 in RCC cells. |
| Pubmed ID | 30226576 |
| Year | 2018 |
| Title | Long Non-Coding RNA HOTTIP Promotes Renal Cell Carcinoma Progression Through the Regulation of the miR-615/IGF-2 Pathway |
External Links
| Links for HOTTIP | GenBank HGNC NONCODE |
| Links for renal cell carcinoma | OMIM COSMIC |