Basic Information
| LncRNA/CircRNA Name | H19 |
| Synonyms | H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 |
| Region | GRCh38_11:1995176-2001470 |
| Ensemble | ENSG00000130600 |
| Refseq | NR_002196 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | 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 blo, Luciferase reporter assay, other |
| Sample | NSCLC tissues andadenocarcinoma cell line (A549, SPC-A1) ,squamous cell line (SKMES-1) |
| Expression Pattern | up-regulated |
| Function Description | It was also found that patients who were in advanced clinical stages had a higher H19 and a lower miR-203 expression compared to normal tissues. The overall survival time of patients with higher H19 expression was shorter compared with the lower H19 expression group. Upregulation of A549 enhanced cell proliferation and promoted invasion. Overexpression of H19 stimulated the epithelial-mesenchymal transition (EMT) process in lung cancer cells and demonstrated typical morphological characteristics of EMT. The level of mesenchymal marker protein, such as Vimentin and SNAI1 increased; while CDH1 protein level decreased. Also, H19 negatively regulated miR-203. Inhibition of H19 attenuated miR-203 induced EMT process. |
| Pubmed ID | 30214583 |
| Year | 2018 |
| Title | H19 Contributes to Poor Clinical Features in NSCLC Patients and Leads to Enhanced Invasion in A549 Cells Through Regulating miRNA-203-mediated Epithelial-Mesenchymal Transition |
External Links
| Links for H19 | GenBank HGNC NONCODE |
| Links for non small cell lung cancer | OMIM COSMIC |