Basic Information
LncRNA/CircRNA Name | BCAR4 |
Synonyms | NA |
Region | GRCh38_16:11819829-11828845 |
Ensemble | ENSG00000262117 |
Refseq | NR_024049 |
Classification Information
Regulatory Mechanism | Biological Function | Clinical Application | |||
---|---|---|---|---|---|
TF | Immune | Survival | |||
Enhancer | Apoptosis | Drug | Tamoxifen | ||
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, Luciferase reporter assay, in vitro knockdown, etc. |
Sample | CRPC tissues, human PC cell lines (PC346, LNCap, BPH1, MDAPC1 2a/b, C4-2, PC3 and DU145) |
Expression Pattern | up-regulated |
Function Description | a lncRNA, Breast-Cancer Anti-Estrogen Resistance 4 (BCAR4), which plays a pivotal role in the tamoxifen-resistance of breast cancer, was significantly upregulated in CRPC, but not in castration-sensitive prostate cancer (CSPC), compared to normal prostate tissue. High BCAR4 levels in CRPC were correlated with poor patients overall survival. Androgen increased growth and migration of androgen receptor (AR)-positive PC346 cells, which was abolished by the antagonist of androgen. Overexpression of BCAR4 in PC346 cells increased cell growth and migration, but turned the cells insensitive to androgen. On the other hand, growth and migration of AR-negative DU145 cells are insensitive to androgen, while depletion of BCAR4 in DU145 cells not only decreased cell growth, but also turned the cells sensitive again to androgen. Moreover, BCAR4 activated GLI2 downstream genes, and correlated with the levels of these GLI2-target genes in CRPC. Depletion of GLI2 abolished the effects of BCAR4 on cell growth and migration. |
Pubmed ID | 30513511 |
Year | 2018 |
Title | BCAR4 activates GLI2 signaling in prostate cancer to contribute to castration resistance |
External Links
Links for BCAR4 | GenBank HGNC NONCODE |
Links for prostate cancer | OMIM COSMIC |