CUL4B and KDM5B ChIP-sequencing in MCF-7 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE286885 | GEO | 2026/02/18
REPOSITORIES: GEO
Similar Datasets
Project description:Cullin 4B (CUL4B) is a scaffold protein of the CUL4B-Ring E3 ligase (CRL4B) complex. Here, we found that CRL4B interacted with transcriptional corepressor complexes. Our results supporting CUL4B as a potential target of cancer therapy.
2021-03-25 | GSE124611 | GEO
Project description:The KDM5B histone H3 lysine 4 (H3K4) demethylase has been implicated in therapy resistance in multiple cancer types including breast cancer, but the underlying mechanism is poorly defined. Here we show that inhibition of KDM5B activity increases sensitivity to anti-estrogens by modulating estrogen-receptor (ER) signaling. Conversely, acquired resistance to KDM5 inhibitors leads to gain of ER chromatin binding and estrogen-independent growth. Sequencing of barcoded cell populations and mathematical modeling demonstrate selection for pre-existent genetically distinct endocrine-resistant cells, while resistance to KDM5 inhibitors is a switch to an acquired epigenetic state. Rare resistant cells can already be detected by single cell RNA-seq prior to treatment. Inhibition of KDM5B in luminal ER+ cells increases H3K4me3 broad domains at promoters and decreases cellular transcriptional heterogeneity. Higher transcriptome heterogeneity is associated with higher KDM5B levels and poor prognosis in ER+ luminal breast tumors.
2018-10-03 | GSE104981 | GEO
Project description:The KDM5B histone H3 lysine 4 (H3K4) demethylase has been implicated in therapy resistance in multiple cancer types including breast cancer, but the underlying mechanism is poorly defined. Here we show that inhibition of KDM5B activity increases sensitivity to anti-estrogens by modulating estrogen-receptor (ER) signaling. Conversely, acquired resistance to KDM5 inhibitors leads to gain of ER chromatin binding and estrogen-independent growth. Sequencing of barcoded cell populations and mathematical modeling demonstrate selection for pre-existent genetically distinct endocrine-resistant cells, while resistance to KDM5 inhibitors is a switch to an acquired epigenetic state. Rare resistant cells can already be detected by single cell RNA-seq prior to treatment. Inhibition of KDM5B in luminal ER+ cells increases H3K4me3 broad domains at promoters and decreases cellular transcriptional heterogeneity. Higher transcriptome heterogeneity is associated with higher KDM5B levels and poor prognosis in ER+ luminal breast tumors.
2018-10-03 | GSE104987 | GEO
Project description:The KDM5B histone H3 lysine 4 (H3K4) demethylase has been implicated in therapy resistance in multiple cancer types including breast cancer, but the underlying mechanism is poorly defined. Here we show that inhibition of KDM5B activity increases sensitivity to anti-estrogens by modulating estrogen-receptor (ER) signaling. Conversely, acquired resistance to KDM5 inhibitors leads to gain of ER chromatin binding and estrogen-independent growth. Sequencing of barcoded cell populations and mathematical modeling demonstrate selection for pre-existent genetically distinct endocrine-resistant cells, while resistance to KDM5 inhibitors is a switch to an acquired epigenetic state. Rare resistant cells can already be detected by single cell RNA-seq prior to treatment. Inhibition of KDM5B in luminal ER+ cells increases H3K4me3 broad domains at promoters and decreases cellular transcriptional heterogeneity. Higher transcriptome heterogeneity is associated with higher KDM5B levels and poor prognosis in ER+ luminal breast tumors.
2018-10-03 | GSE104986 | GEO
Project description:The KDM5B histone H3 lysine 4 (H3K4) demethylase has been implicated in therapy resistance in multiple cancer types including breast cancer, but the underlying mechanism is poorly defined. Here we show that inhibition of KDM5B activity increases sensitivity to anti-estrogens by modulating estrogen-receptor (ER) signaling. Conversely, acquired resistance to KDM5 inhibitors leads to gain of ER chromatin binding and estrogen-independent growth. Sequencing of barcoded cell populations and mathematical modeling demonstrate selection for pre-existent genetically distinct endocrine-resistant cells, while resistance to KDM5 inhibitors is a switch to an acquired epigenetic state. Rare resistant cells can already be detected by single cell RNA-seq prior to treatment. Inhibition of KDM5B in luminal ER+ cells increases H3K4me3 broad domains at promoters and decreases cellular transcriptional heterogeneity. Higher transcriptome heterogeneity is associated with higher KDM5B levels and poor prognosis in ER+ luminal breast tumors.
2018-10-03 | GSE104983 | GEO
Project description:The KDM5B histone H3 lysine 4 (H3K4) demethylase has been implicated in therapy resistance in multiple cancer types including breast cancer, but the underlying mechanism is poorly defined. Here we show that inhibition of KDM5B activity increases sensitivity to anti-estrogens by modulating estrogen-receptor (ER) signaling. Conversely, acquired resistance to KDM5 inhibitors leads to gain of ER chromatin binding and estrogen-independent growth. Sequencing of barcoded cell populations and mathematical modeling demonstrate selection for pre-existent genetically distinct endocrine-resistant cells, while resistance to KDM5 inhibitors is a switch to an acquired epigenetic state. Rare resistant cells can already be detected by single cell RNA-seq prior to treatment. Inhibition of KDM5B in luminal ER+ cells increases H3K4me3 broad domains at promoters and decreases cellular transcriptional heterogeneity. Higher transcriptome heterogeneity is associated with higher KDM5B levels and poor prognosis in ER+ luminal breast tumors.
2018-10-03 | GSE104984 | GEO
Project description:The KDM5B histone H3 lysine 4 (H3K4) demethylase has been implicated in therapy resistance in multiple cancer types including breast cancer, but the underlying mechanism is poorly defined. Here we show that inhibition of KDM5B activity increases sensitivity to anti-estrogens by modulating estrogen-receptor (ER) signaling. Conversely, acquired resistance to KDM5 inhibitors leads to gain of ER chromatin binding and estrogen-independent growth. Sequencing of barcoded cell populations and mathematical modeling demonstrate selection for pre-existent genetically distinct endocrine-resistant cells, while resistance to KDM5 inhibitors is a switch to an acquired epigenetic state. Rare resistant cells can already be detected by single cell RNA-seq prior to treatment. Inhibition of KDM5B in luminal ER+ cells increases H3K4me3 broad domains at promoters and decreases cellular transcriptional heterogeneity. Higher transcriptome heterogeneity is associated with higher KDM5B levels and poor prognosis in ER+ luminal breast tumors.
2018-10-03 | GSE104985 | GEO
Project description:It has been reported that PHF1, CUL4B and PRMT5 all play important roles in epigenetic regulation. We reported that PHF1, CRL4B and PRMT5 may act as a complex in transcriptional regulation and have a vital effect in breast cancer progression. So we performed ChIP-on-chip assays to find unique promoters co-targeted by PHF1, CUL4B and PRMT5. PHF1, CUL4B and PRMT5 have a predominant cooperation, at least in MDA-MB-231 cells. comparison of PHF1, CUL4B and PRMT5 target genes
2016-07-07 | E-GEOD-84071 | biostudies-arrayexpress
Project description:It has been reported that PHF1, CUL4B and PRMT5 all play important roles in epigenetic regulation. We reported that PHF1, CRL4B and PRMT5 may act as a complex in transcriptional regulation and have a vital effect in breast cancer progression. So we performed ChIP-on-chip assays to find unique promoters co-targeted by PHF1, CUL4B and PRMT5. PHF1, CUL4B and PRMT5 have a predominant cooperation, at least in MDA-MB-231 cells.
2016-07-07 | GSE84071 | GEO
Project description:Approximately 30% of cases are resistant to TAM, which has become a major obstacle for breast cancer therapy.In this study, we demonstrated that CUL4B promotes TAM resistance in breast cancer cells through miR-32-5p/ER-α36 axis. CUL4B is overexpressed in TAM-resistant breast cancer cells and positively correlates with the levels of ER-α36 protein in human breast cancer specimens. Mechanistically, CUL4B positively regulates ER-α36 expression by epigenetically repressing the transcription of miR-32-5p. These findings provide not only a mechanistic insight into the role of CUL4B in regulating TAM sensitivity but also a potential target for the therapy of breast cancer.
2022-09-08 | GSE158651 | GEO