Basic Information
| LncRNA/CircRNA Name | LSINCT5 |
| Synonyms | NA |
| Region | GRCh38_5:2712591-2715237 |
| Ensemble | |
| Refseq | NR_145480 |
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 | hepatocellular carcinoma |
| ICD-0-3 | C22.0 |
| Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP, etc. |
| Sample | HCC tumor tissues, The HCC cell lines 97L, HepG2, Hep3B, 7721, and Huh7, the 293T cells, and the normal human hepatocyte L02 cells |
| Expression Pattern | up-regulated |
| Function Description | identified a novel lncRNA named long stress induced non-coding transcripts 5 (LSINCT5) which facilitates HCC progression. LSINCT5 was significantly upregulated in both HCC specimens and cell lines and correlates with poor survival. In vitro experiments showed that LSINCT5 promoted migration and viability of HepG2 and Huh7 cells. The in vivo xenograft mouse model also confirmed an oncogenic role for LSINCT5. RIP in combination with mass spectrometry identified HMGA2 as the LSINCT5 binding partner. LSINCT5 could bind to HMGA2 and decrease proteasome-mediated HMGA2 degradation leading to EMT activation. LSINCT5 also served as a competing endogenous RNA (ceRNA) for miR-4516, resulting in increased STAT3/BclxL expression and attenuated apoptosis |
| Pubmed ID | 30472720 |
| Year | 2018 |
| Title | Long Stress Induced Non-Coding Transcripts 5 (LSINCT5) Promotes Hepatocellular Carcinoma Progression Through Interaction with HighMobility Group AT-hook 2 and MiR-4516 |
External Links
| Links for LSINCT5 | GenBank HGNC NONCODE |
| Links for hepatocellular carcinoma | OMIM COSMIC |