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Title:
Regulatory mechanisms of steroid hormone receptors on gene transcription through chromatin interaction and enhancer reprogramming | Cellular Oncology
Description:
Regulation of steroid hormone receptors (SHRs) on transcriptional reprogramming is crucial for breast cancer progression. SHRs, including estrogen receptor (ER), androgen receptor (AR), progesterone receptor (PR), and glucocorticoid receptor (GR) play key roles in remodeling the transcriptome of breast cancer cells. However, the molecular mechanisms by which SHRs regulate chromatin landscape in enhancer regions and transcription factor interactions remain largely unknown. In this review, we summarized the regulatory effects of 3 types of SHRs (AR, PR, and GR) on gene transcription through chromatin interactions and enhancer reprogramming. Specifically, AR and PR exhibit bi-directional regulatory effects (both inhibitory and promoting) on ER-mediated gene transcription, while GR modulates the transcription of pro-proliferation genes in ER-positive breast cancer cells. In addition, we have presented four enhancer reprogramming mechanisms (transcription factor cooperation, pioneer factor binding, dynamic assisted loading, and tethering) and the multiple enhancer-promoter contact models. Based on these mechanisms and models, this review proposes that the combination of multiple therapy strategies such as agonists/antagonists of SHRs plus endocrine therapy and the adoption of the latest sequencing technologies are expected to improve the efficacy of ER positive breast cancer treatment.
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Keywords {๐}
pubmed, article, google, scholar, cas, central, cancer, breast, receptor, cell, mol, transcription, glucocorticoid, estrogen, enhancer, biol, res, transcriptional, gene, chromatin, cells, nat, androgen, progesterone, sci, receptors, factor, binding, human, expression, reprogramming, activation, factors, nature, activity, eralpha, mechanisms, steroid, hormone, function, genome, foxa, action, protein, endocrinol, regulation, response, genet, commun, complex,
Topics {โ๏ธ}
enhancer-driven lineage-specific transcription illumina-based chip-exonuclease method ezh2-eralpha-greb1 transcriptional axis estrogen-receptor-positive breast cancer high-resolution data shows month download article/chapter articleย google scholar hormone-induced breast cancer er-dependent gene expression her2-positive breast carcinomas lymphocyte-specific cellular enhancer estrogen receptor-dependent transcription er-positive breast cancer progestin-driven mammary cancer ligand-inducible growth state protein-nucleic acid complexes er-mediated gene transcription estrogen receptor-sp1 interactions oestrogen-dependent transcriptional activation retinoic acid receptor-alpha direct/indirect dna recruitment promote chromatin-based regulation oncogenic super-enhancer formation anti-diabetic drug response transcription factors access er-negative breast cancer full article pdf modulate oncogene-induced senescence endocrine-resistant breast cancer mutant estrogen receptors eralpha-regulated transcriptional program apolipoprotein-mediated cholesterol efflux pelp1-mediated stress signaling agonist-liganded glucocorticoid receptor triple-negative breast cancer cytokine-mediated endocrine resistance receptor-mediated transcriptional activation long-term clinical benefit foxa1/esr1 interacting pathway eralpha/sp1-mediated activation foxa1-dna binding properties direct cell-fate conversion related subjects cyclin d1/myc promoters myc/max/mad network promoting enhancer-promoter interaction 3d chromatin architecture fluorescence cross-correlation spectroscopy estrogen receptor cistrome estrogen receptor alpha
Questions {โ}
- Newton, Molecular mechanisms of glucocorticoid action: what is important?
- Prekovic, Duality of glucocorticoid action in cancer: tumor-suppressor or oncogene?
- Wysocka, Modification of enhancer chromatin: what, how, and why?
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headline:Regulatory mechanisms of steroid hormone receptors on gene transcription through chromatin interaction and enhancer reprogramming
description:Regulation of steroid hormone receptors (SHRs) on transcriptional reprogramming is crucial for breast cancer progression. SHRs, including estrogen receptor (ER), androgen receptor (AR), progesterone receptor (PR), and glucocorticoid receptor (GR) play key roles in remodeling the transcriptome of breast cancer cells. However, the molecular mechanisms by which SHRs regulate chromatin landscape in enhancer regions and transcription factor interactions remain largely unknown. In this review, we summarized the regulatory effects of 3 types of SHRs (AR, PR, and GR) on gene transcription through chromatin interactions and enhancer reprogramming. Specifically, AR and PR exhibit bi-directional regulatory effects (both inhibitory and promoting) on ER-mediated gene transcription, while GR modulates the transcription of pro-proliferation genes in ER-positive breast cancer cells. In addition, we have presented four enhancer reprogramming mechanisms (transcription factor cooperation, pioneer factor binding, dynamic assisted loading, and tethering) and the multiple enhancer-promoter contact models. Based on these mechanisms and models, this review proposes that the combination of multiple therapy strategies such as agonists/antagonists of SHRs plus endocrine therapy and the adoption of the latest sequencing technologies are expected to improve the efficacy of ER positive breast cancer treatment.
datePublished:2024-11-14T00:00:00Z
dateModified:2024-11-14T00:00:00Z
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Enhancer
Breast cancer
Estrogen receptor
Steroid hormone receptors
Enhancer reprogramming
Cancer Research
Biomedicine
general
Pathology
Oncology
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headline:Regulatory mechanisms of steroid hormone receptors on gene transcription through chromatin interaction and enhancer reprogramming
description:Regulation of steroid hormone receptors (SHRs) on transcriptional reprogramming is crucial for breast cancer progression. SHRs, including estrogen receptor (ER), androgen receptor (AR), progesterone receptor (PR), and glucocorticoid receptor (GR) play key roles in remodeling the transcriptome of breast cancer cells. However, the molecular mechanisms by which SHRs regulate chromatin landscape in enhancer regions and transcription factor interactions remain largely unknown. In this review, we summarized the regulatory effects of 3 types of SHRs (AR, PR, and GR) on gene transcription through chromatin interactions and enhancer reprogramming. Specifically, AR and PR exhibit bi-directional regulatory effects (both inhibitory and promoting) on ER-mediated gene transcription, while GR modulates the transcription of pro-proliferation genes in ER-positive breast cancer cells. In addition, we have presented four enhancer reprogramming mechanisms (transcription factor cooperation, pioneer factor binding, dynamic assisted loading, and tethering) and the multiple enhancer-promoter contact models. Based on these mechanisms and models, this review proposes that the combination of multiple therapy strategies such as agonists/antagonists of SHRs plus endocrine therapy and the adoption of the latest sequencing technologies are expected to improve the efficacy of ER positive breast cancer treatment.
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Breast cancer
Estrogen receptor
Steroid hormone receptors
Enhancer reprogramming
Cancer Research
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Oncology
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