Enhancer ID: | E_02_0269 |
Species: | human |
Position : | chr3:181709362-181711362 |
Biosample name: | |
Experiment class : | High+Lowthroughput |
Enhancer type: | Enhancer |
Disease: | Prostate cancer |
Pubmed ID: | 30952632 |
Enhancer experiment: | Immunofluorescence staining, immunohistochemistry |
Enhancer experiment description: | The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,2) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generation AR antagonist enzalutamide (Enz), or the androgen-biosynthesis inhibitor abiraterone acetate (37). Further, elevated expression of the glucocorticoid receptor can bypass dependence on the AR by promiscuously activating AR target genes (8) or through lineage plasticity driven by SOX2 |
Target gene : | SOX2(ANOP3,MCOPS3),SOX3,SOX4 |
Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
Less strong evidence: | RNA-Seq |
Target gene experiment description: | The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,2) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generation AR antagonist enzalutamide (Enz), or the androgen-biosynthesis inhibitor abiraterone acetate (37). Further, elevated expression of the glucocorticoid receptor can bypass dependence on the AR by promiscuously activating AR target genes (8) or through lineage plasticity driven by SOX2;The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,3) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat;The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,4) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat& |
TF name : | -- |
TF experiment: | ??????????? |
TF experiment description: | The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,2) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generation AR antagonist enzalutamide (Enz), or the androgen-biosynthesis inhibitor abiraterone acetate (37). Further, elevated expression of the glucocorticoid receptor can bypass dependence on the AR by promiscuously activating AR target genes (8) or through lineage plasticity driven by SOX2;The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,3) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat;The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,4) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat& |
Enhancer function : | The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,2) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generation AR antagonist enzalutamide (Enz), or the androgen-biosynthesis inhibitor abiraterone acetate (37). Further, elevated expression of the glucocorticoid receptor can bypass dependence on the AR by promiscuously activating AR target genes (8) or through lineage plasticity driven by SOX2 |
Enhancer function experiment: | Immunohistochemical staining |
Enhancer function experiment description: |
The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,2) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generation AR antagonist enzalutamide (Enz), or the androgen-biosynthesis inhibitor abiraterone acetate (37). Further, elevated expression of the glucocorticoid receptor can bypass dependence on the AR by promiscuously activating AR target genes (8) or through lineage plasticity driven by SOX2 |
SNP ID: | -- |
GeneName | Pathway Name | Source | Gene Number |
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