Basic Information
LncRNA/CircRNA Name | NEAT1 |
Synonyms | NA |
Region | GRCh38_11:65422774-65445540 |
Ensemble | ENSG00000245532 |
Refseq | NR_028272 |
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 | glioma |
ICD-0-3 | NA |
Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP, etc. |
Sample | Normal human astrocytes (NHAs), U251, U87, SW1783, LN229, and MO59J cells |
Expression Pattern | up-regulated |
Function Description | NEAT1 was greatly upregulated in glioma cells compared with normal human astrocytes (NHAs). Meanwhile, miR 107 was significantly downregulated in glioma cell lines. Then, we observed that knockdown of NEAT1 suppressed the growth and invasion of glioma cells including U251 and SW1783 cells. Reversely, overexpression of NEAT1 dramatically induced glioma cell survival, increased cell colony formation, and promoted cell invasion ability. Subsequently, bioinformatics analysis was performed to predict the correlation between NEAT1 and miR 107. Moreover, it was revealed that NEAT1 could modulate miR 107 via serving as an endogenous sponge of miR 107. The direct binding correlation between NEAT1 and miR 107 was validated in our study. In addition, cyclin dependent kinase 14 (CDK14) was predicted as an messenger RNA target of miR 107 and the association between them was confirmed in our research. Moreover, we implied that NEAT1 demonstrated its biological functions via regulating miR 107 and CDK14 in vivo |
Pubmed ID | 30480816 |
Year | 2018 |
Title | Knockdown of NEAT1 repressed the malignant progression of glioma through sponging miR-107 and inhibiting CDK14 |
External Links
Links for NEAT1 | GenBank HGNC NONCODE |
Links for glioma | OMIM COSMIC |