| Enhancer ID: | E_01_0487 |
| Species: | human |
| Position : | chr7:152132016-152134016 |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Mammary cancer |
| Pubmed ID: | 29755131 |
| Enhancer experiment: | CRISPR/Cas9,next-generation sequencing (IMPACT) assay,Proliferation assays,Immunoblotting,Lentiviral Infections,Quantitative RT-PCR,Chromatin Immunoprecipitation,Immunohistochemistry,Rapid immunoprecipitation mass spectrometry of endogenous proteins (RIME),Chromatin Immunoprecipitation followed by sequencing, |
| Enhancer experiment description: | From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance. |
| Target gene : | -- |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance.;From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance. |
| TF name : | KMT2CFOXA1(HNF3A,TCF3A) |
| TF experiment: | CRISPR/Cas9,next-generation sequencing (IMPACT) assay,Proliferation assays,Immunoblotting,Lentiviral Infections,Quantitative RT-PCR,Chromatin Immunoprecipitation,Immunohistochemistry,Rapid immunoprecipitation mass spectrometry of endogenous proteins (RIME),Chromatin Immunoprecipitation followed by sequencing, |
| TF experiment description: | From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance.;From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance. |
| Enhancer function : | From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance. |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance. |
| SNP ID: | -- |
| GeneName | Pathway Name | Source | Gene Number |
|---|---|---|---|
| KMT2C | Activation of anterior HOX genes in hindbrain development during early embryogenesis | reactome | 120 |
| KMT2C | PKMTs methylate histone lysines | reactome | 64 |
| FOXA1 | AndrogenReceptor | netpath | 167 |
| FOXA1 | Direct p53 effectors | pid | 141 |
| FOXA1 | FOXA1 transcription factor network | pid | 45 |
| FOXA1 | FOXA2 and FOXA3 transcription factor networks | pid | 45 |
| FOXA1 | Hs_Endoderm_Differentiation_WP2853_88152 | wikipathways | 62 |