Basic Information
| LncRNA/CircRNA Name | NLUCAT1 |
| Synonyms | NA |
| Region | NA |
| Ensemble | NA |
| Refseq | NA |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | apoptosis | Drug | Cisplatin | |
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | lung adenocarcinoma |
| ICD-0-3 | C34 |
| Methods | qPCR, Microarray, RNA-seq, other |
| Sample | LUAD tissues and cell lines (A549, H1975, and H2228) |
| Expression Pattern | up-regulated |
| Function Description | Full molecular characterization showed that NLUCAT1 is a large nuclear transcript composed of six exons and mainly regulated by NF-?B and NRF2 transcription factors. CRISPR-Cas9-mediated invalidation of NLUCAT1 revealed a decrease in proliferative and invasive properties, an increase in oxidative stress and a higher sensitivity to cisplatin-induced apoptosis. Transcriptome analysis of NLUCAT1-deficient cells showed repressed genes within the antioxidant and/or cisplatin-response networks. We demonstrated that the concomitant knockdown of four of these genes products, GPX2, GLRX, ALDH3A1, and PDK4, significantly increased ROS-dependent caspase activation, thus partially mimicking the consequences of NLUCAT1 inactivation in LUAD cells. |
| Pubmed ID | 31417181 |
| Year | 2019 |
| Title | The Nuclear Hypoxia-Regulated NLUCAT1 Long Non-Coding RNA Contributes to an Aggressive Phenotype in Lung Adenocarcinoma Through Regulation of Oxidative Stress |
External Links
| Links for NLUCAT1 | GenBank HGNC NONCODE |
| Links for lung adenocarcinoma | OMIM COSMIC |