Basic Information
| LncRNA/CircRNA Name | PCAT9 |
| Synonyms | PCGEM1, LINC00071, NCRNA00071, PCAT9 |
| Region | GRCh38_2:192749845-192776899 |
| Ensemble | ENSG00000227418 |
| Refseq | NR_002769 |
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 | prostate cancer |
| ICD-0-3 | C61.9 |
| Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown |
| Sample | prostate cancer cell lines(LNCaP and 22Rv1) |
| Expression Pattern | up-regulated |
| Function Description | knockdown of PCAT3 and PCAT9 suppressed cellular proliferation, invasion, migration, angiogenesis and stemness in androgen-dependent LNCaP and 22Rv1 cells. both PCAT3 and PCAT9 transcripts had two conserved binding sties for miR-203. Meanwhile, dual luciferase report assays revealed that miR-203 could suppress the luciferase activities of reporter plasmids carrying the binding site of miR-203 on the mRNA of PCAT3 or PCAT9. Quantitative RT-PCR (qRT-PCR) and RNA fluorescence in situ hybridization (RNA-FISH) showed that miR-203 mimic reduced the expression of PCAT3 and PCAT9 both in LNCaP and 22Rv1 cells. We also noted that both PCAT3 and PCAT9 inhibited miR-203 expression and alleviated repression on the expression of SNAI2, a critical regulator of epithelial-mesenchymal transition directly targeted by miR-203. |
| Pubmed ID | 29552304 |
| Year | 2018 |
| Title | The PCAT3/PCAT9-miR-203-SNAI2 axis functions as a key mediator for prostate tumor growth and progression. |
External Links
| Links for PCAT9 | GenBank HGNC NONCODE |
| Links for prostate cancer | OMIM COSMIC |