ArticleMolecular and cellular biology2012
CBP mediates NF-κB-dependent histone acetylation and estrogen receptor recruitment to an estrogen response element in the BIRC3 promoter.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Novel ceRNA network construction associated with programmed cell death in acute rejection of heart allograft in mice.Frontiers in immunology · 2023Article
- Estrogen Receptor-Regulated Gene Signatures in Invasive Breast Cancer Cells and Aggressive Breast Tumors.Cancers · 2022Article
- Estrogen Receptor Alpha and ESR1 Mutations in Breast Cancer.Advances in experimental medicine and biology · 2022Article
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- Targeting Histone Modifications in Breast Cancer: A Precise Weapon on the Way.Frontiers in cell and developmental biology · 2021Review
- Estrogen Receptor Beta Influences the Inflammatory p65 Cistrome in Colon Cancer Cells.Frontiers in endocrinology · 2021Article
- Update on the Role of NFκB in Promoting Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer.Endocrinology · 2020Review
- Histone deacetylase inhibitors suppress transdifferentiation of gonadotrophs to prolactin cells and proliferation of prolactin cells induced by diethylstilbestrol in male mouse pituitary.Histochemistry and cell biology · 2019Article
- Signaling pathways and steroid receptors modulating estrogen receptor α function in breast cancer.Genes & development · 2018Review
- Differential expression of genes in HepG2 cells caused by UC001kfo RNAi as shown by RNA-seq.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017Article
- A Novel Strategy to Co-target Estrogen Receptor and Nuclear Factor κB Pathways with Hybrid Drugs for Breast Cancer Therapy.Hormones & cancer · 2017Article
- Structural and Molecular Mechanisms of Cytokine-Mediated Endocrine Resistance in Human Breast Cancer Cells.Molecular cell · 2017Article
- ROR1 is essential for proper innervation of auditory hair cells and hearing in humans and mice.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Dimethyl Fumarate Inhibits the Nuclear Factor κB Pathway in Breast Cancer Cells by Covalent Modification of p65 Protein.The Journal of biological chemistry · 2016Article
- PADI2 gene confers susceptibility to breast cancer and plays tumorigenic role via ACSL4, BINC3 and CA9 signaling.Cancer cell international · 2016Article
- NFκB affects estrogen receptor expression and activity in breast cancer through multiple mechanisms.Molecular and cellular endocrinology · 2015Review
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- A novel aspirin prodrug inhibits NFκB activity and breast cancer stem cell properties.BMC cancer · 2015Article
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Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Estrogen receptor (ER) and NF-κB are transcription factors with profound effects on breast cancer cell proliferation and survival. While many studies demonstrate that ER and NF-κB can repress each other, we previously identified a gene signature that is synergistically upregulated by these two factors in more aggressive luminal B breast tumors. Herein, we examine a novel mechanism of cross talk between ER and NF-κB that results in the upregulation of the antiapoptotic gene BIRC3 (also known as cIAP2). We demonstrate that NF-κB, acting through two response elements, is required for ER recruitment to an adjacent estrogen response element (ERE) in the BIRC3 promoter. This effect is accompanied by a major increase in NF-κB-dependent histone acetylation around the ERE. Interestingly, CBP, a histone acetyltransferase previously implicated in repressive interactions between ER and NF-κB, plays a permissive role by promoting histone acetylation and ER recruitment, as well as enhanced expression of BIRC3. These findings suggest a new gene regulatory mechanism by which inflammation and NF-κB activation can influence ER recruitment to inherently inactive ER binding sites. This fine-tuning mechanism may explain how two factors that generally repress each other's activity may work together on certain genes to promote breast cancer cell survival and tumor progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.