ArticleThe Journal of biological chemistry2017
Histone H1 and Chromosomal Protein HMGN2 Regulate Prolactin-induced STAT5 Transcription Factor Recruitment and Function in Breast Cancer Cells.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- The Roles of STAT3 and STAT5 in Breast Cancer.Cancers · 2025Review
- HMGN2 accelerates the proliferation and cell cycle progression of glioblastoma by regulating CDC20 expression.Genes & diseases · 2025Article
- Deficiency of HMGN2 enhances antibacterial activity of macrophages by promoting H3 histone modification-mediated CD14/iNOS expression.Frontiers in immunology · 2025Article
- Chromatin accessibility: biological functions, molecular mechanisms and therapeutic application.Signal transduction and targeted therapy · 2024Review
- HMGN1 loss sensitizes lung cancer cells to chemotherapy.Scientific reports · 2024Article
- Progress in Research on Key Factors Regulating Lactation Initiation in the Mammary Glands of Dairy Cows.Genes · 2023Review
- HMGN2 and Histone H1.2: potential targets of a novel probiotic mixture for seasonal allergic rhinitis.Frontiers in microbiology · 2023Article
- STAT family of transcription factors in breast cancer: Pathogenesis and therapeutic opportunities and challenges.Seminars in cancer biology · 2022Review
- Novel biomarkers predict prognosis and drug-induced neuroendocrine differentiation in patients with prostate cancer.Frontiers in endocrinology · 2022Article
- Serine residues 726 and 780 have nonredundant roles regulating STAT5a activity in luminal breast cancer.Scientific reports · 2021Article
- Site-specific modification and segmental isotope labelling of HMGN1 reveals long-range conformational perturbations caused by posttranslational modifications.RSC chemical biology · 2021Article
- Histone Deacetylase Inhibitor Trichostatin A Reduces Endothelial Cell Proliferation by Suppressing STAT5A-Related Gene Transcription.Frontiers in oncology · 2021Article
- Involvement of STAT5 in Oncogenesis.Biomedicines · 2020Review
- Systems biology comprehensive analysis on breast cancer for identification of key gene modules and genes associated with TNM-based clinical stages.Scientific reports · 2020Article
- Exogenous HMGN2 inhibits the migration and invasion of osteosarcoma cell lines.Translational cancer research · 2020Article
- Biological Functions of HMGN Chromosomal Proteins.International journal of molecular sciences · 2020Review
- Effect of HMGN2 on proliferation and apoptosis of MCF-7 breast cancer cells.Oncology letters · 2019Article
- Trisomy of a Down Syndrome Critical Region Globally Amplifies Transcription via HMGN1 Overexpression.Cell reports · 2018Article
- HMGN1 and 2 remodel core and linker histone tail domains within chromatin.Nucleic acids research · 2017Article
- The transcriptional STAT3 is a potential target, whereas transcriptional STAT5A/5B/6 are new biomarkers for prognosis in human breast carcinoma.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The hormone prolactin (PRL) contributes to breast cancer pathogenesis through various signaling pathways, one of the most notable being the JAK2/signal transducer and activator of transcription 5 (STAT5) pathway. PRL-induced activation of the transcription factor STAT5 results in the up-regulation of numerous genes implicated in breast cancer pathogenesis. However, the molecular mechanisms that enable STAT5 to access the promoters of these genes are not well understood. Here, we show that PRL signaling induces chromatin decompaction at promoter DNA, corresponding with STAT5 binding. The chromatin-modifying protein high mobility group nucleosomal binding domain 2 (HMGN2) specifically promotes STAT5 accessibility at promoter DNA by facilitating the dissociation of the linker histone H1 in response to PRL. Knockdown of H1 rescues the decrease in PRL-induced transcription following HMGN2 knockdown, and it does so by allowing increased STAT5 recruitment. Moreover, H1 and STAT5 are shown to function antagonistically in regulating PRL-induced transcription as well as breast cancer cell biology. While reduced STAT5 activation results in decreased PRL-induced transcription and cell proliferation, knockdown of H1 rescues both of these effects. Taken together, we elucidate a novel mechanism whereby the linker histone H1 prevents STAT5 binding at promoter DNA, and the PRL-induced dissociation of H1 mediated by HMGN2 is necessary to allow full STAT5 recruitment and promote the biological effects of PRL signaling.
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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.