ArticleMolecular endocrinology (Baltimore, Md.)2008
A conserved molecular mechanism is responsible for the auto-up-regulation of glucocorticoid receptor gene promoters.
Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 41 citations in OpenAlex.
- The Glucocorticoid Receptor: Isoforms, Functions, and Contribution to Glucocorticoid Sensitivity.Endocrine reviews · 2024Review
- Silibinin, an HSP90 Inhibitor, on Human ACTH-Secreting Adenomas.Neuroendocrinology · 2023Article
- Article
- Epigenetic alteration by DNA-demethylating treatment restores apoptotic response to glucocorticoids in dexamethasone-resistant human malignant lymphoid cells.Cancer cell international · 2014Article
- Direct reversal of glucocorticoid resistance by AKT inhibition in acute lymphoblastic leukemia.Cancer cell · 2013Article
- P300 regulates the human RLIP76 promoter activity and gene expression.Biochemical pharmacology · 2013Article
- Contribution of FKBP5 genetic variation to gemcitabine treatment and survival in pancreatic adenocarcinoma.PloS one · 2013Article
- Role of the hypothalamic-pituitary-adrenal axis in developmental programming of health and disease.Frontiers in neuroendocrinology · 2013Review
- MicroRNAs and Glucocorticoid-Induced Apoptosis in Lymphoid Malignancies.ISRN hematology · 2013Article
- c-Myb interacts with the glucocorticoid receptor and regulates its level in pre-B-acute lymphoblastic leukemia cells.Molecular and cellular endocrinology · 2012Article
- A facile, branched DNA assay to quantitatively measure glucocorticoid receptor auto-regulation in T-cell acute lymphoblastic leukemia.Chinese journal of cancer · 2012Article
- Epigenetic changes in fetal hypothalamic energy regulating pathways are associated with maternal undernutrition and twinning.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Transcriptional control of the human glucocorticoid receptor: identification and analysis of alternative promoter regions.Human genetics · 2011Article
- A new, lineage specific, autoup-regulation mechanism for human glucocorticoid receptor gene expression in 697 pre-B-acute lymphoblastic leukemia cells.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Use of recombinant cell-permeable small peptides to modulate glucocorticoid sensitivity of acute lymphoblastic leukemia cells.Biochemistry · 2010Article
- Glucocorticoid receptor knock down reveals a similar apoptotic threshold but differing gene regulation patterns in T-cell and pre-B-cell acute lymphoblastic leukemia.Molecular and cellular endocrinology · 2010Article
- Levels of glucocorticoid receptor and its ligand determine sensitivity and kinetics of glucocorticoid-induced leukemia apoptosis.Leukemia · 2009Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Glucocorticoid (GC) hormones are widely used in the treatment of acute lymphoblastic leukemia (ALL). Whereas a high level of GC receptor (GR) protein is associated with the sensitivity of ALL cells to steroid-mediated apoptosis, the auto-up-regulation of human (h)GR mRNA and protein is also found in hormone-sensitive ALL cell lines. We have characterized the hGR gene-proximal promoters for DNA sequences and transcription factors required for hormone responsiveness in T lymphoblasts. Sequences at -4559/-4525 and -2956/-2916, relative to the translation start site, function as strong composite GC response units (GRUs). Both GRUs include adjacent protein recognition sequences for the c-Myb transcription factor and the GR as a DNA cassette. An Ets-binding sequence overlaps the GR-binding site in the -4559/-4525 GRU, whereas an Ets-binding site present in the -2956/-2916 GRU does not overlap the GR/c-Myb-binding cassette. The Ets protein family member, PU.1, blocks hormonal activation of the -4559/-4525 GR/c-Myb-binding cassette but does not interfere with the responsiveness of the -2956/-2916 GRU. Thus, the hGR 1A GRU (described previously), the -4559/-4525 GRU, and the -2956/-2916 GRU have a similar structure and can mediate cell type-specific hormonal auto-up-regulation of hGR promoter activity in steroid-sensitive ALL cells. However, subtle differences in the GRU architecture result in differential sensitivity of the promoters to Ets family members such as PU.1. The architecture of the GRU and the spectrum of specific transcription factors present in different types of ALL might allow the development of a tailored therapy to enhance steroid sensitivity in ALL patients.
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