Basic Information
LncRNA/CircRNA Name | FTH1P3 |
Synonyms | FTH1P3, FTHL3, FTHL3P |
Region | GRCh38_2:27392784-27393367 |
Ensemble | ENSG00000213453 |
Refseq | NA |
Classification Information
Regulatory Mechanism | Biological Function | Clinical Application | |||
---|---|---|---|---|---|
TF | Immune | Survival | |||
Enhancer | Apoptosis | Drug | Paclitaxel | ||
Variant | Cell Growth | Circulating | |||
MiRNA | EMT | Metastasis | |||
Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
Cancer Name | breast cancer |
ICD-0-3 | C50 |
Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown |
Sample | breast cancer tissues, cell lines (MCF-7, MDA-MB-231, MDA-MB-468, MDA-MB-453) |
Expression Pattern | up-regulated |
Function Description | Results showed that lncRNA FTH1P3 was up-regulated in paclitaxel-resistant breast cancer tissue and cells (MCF-7/PTX and MDA-MB-231/PTX cells) compared with paclitaxel-sensitive tissue and parental cell lines (MCF-7, MDA-MB-231). Gain- and loss-of-function experiments revealed that FTH1P3 silencing decreased the 50% inhibitory concentration (IC50) value of paclitaxel and induced cell cycle arrest at G2/M phase, while FTH1P3-enhanced expression exerted the opposite effects. Bioinformatics tools and luciferase reporter assay validated that FTH1P3 promoted ABCB1 protein expression through targeting miR-206, acting as a miRNA "sponge." |
Pubmed ID | 29971911 |
Year | 2018 |
Title | Long Non-Coding RNA FTH1P3 Activates Paclitaxel Resistance in Breast Cancer Through miR-206/ABCB1 |
External Links
Links for FTH1P3 | GenBank HGNC NONCODE |
Links for breast cancer | OMIM COSMIC |