ArticleOncogene2010
Macrophage migration inhibitory factor is a direct target of HBP1-mediated transcriptional repression that is overexpressed in prostate cancer.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 55 citations in OpenAlex.
- The Research Progress of Tumor-Associated Macrophages in Prostate Cancer.Journal of immunology research · 2026Review
- The role of miR-155 in cardiovascular diseases: Potential diagnostic and therapeutic targets.International journal of cardiology. Cardiovascular risk and prevention · 2025Review
- Impact of particulate microplastics generated from polyethylene terephthalate on gut pathology and immune microenvironments.iScience · 2023Article
- Review
- HBP1 inhibits the development of type 2 diabetes mellitus through transcriptional activation of theAging · 2022Article
- Methylation of HBP1 by PRMT1 promotes tumor progression by regulating actin cytoskeleton remodeling.Oncogenesis · 2022Article
- Pathogenic role of microRNAs in atherosclerotic ischemic stroke: Implications for diagnosis and therapy.Genes & diseases · 2022Review
- miR-335-5P contributes to human osteoarthritis by targeting HBP1.Experimental and therapeutic medicine · 2021Article
- Article
- The HMG box transcription factor HBP1: a cell cycle inhibitor at the crossroads of cancer signaling pathways.Cellular and molecular life sciences : CMLS · 2019Review
- MiR-21 improves invasion and migration of drug-resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1.Cancer medicine · 2018Article
- Novel Insights in the Metabolic Syndrome-induced Oxidative Stress and Inflammation-mediated Atherosclerosis.Current cardiology reviews · 2018Review
- HMG-box transcription factor 1: a positive regulator of the G1/S transition through the Cyclin-CDK-CDKI molecular network in nasopharyngeal carcinoma.Cell death & disease · 2018Article
- MircroRNA-19a promotes vascular inflammation and foam cell formation by targeting HBP-1 in atherogenesis.Scientific reports · 2017Article
- A positive feedback loop between Pim-1 kinase and HBP1 transcription factor contributes to hydrogen peroxide-induced premature senescence and apoptosis.The Journal of biological chemistry · 2017Article
- Transcription factor HBP1 is a direct anti-cancer target of transcription factor FOXO1 in invasive oral cancer.Oncotarget · 2017Article
- Discovering Pair-wise Synergies in Microarray Data.Scientific reports · 2016Article
- HBP1-mediated Regulation of p21 Protein through the Mdm2/p53 and TCF4/EZH2 Pathways and Its Impact on Cell Senescence and Tumorigenesis.The Journal of biological chemistry · 2016Article
- Transcription Factor HBP1 Enhances Radiosensitivity by Inducing Apoptosis in Prostate Cancer Cell Lines.Analytical cellular pathology (Amsterdam) · 2016Article
- HBP1 promoter methylation augments the oncogenic β-catenin to correlate with prognosis in NSCLC.Journal of cellular and molecular medicine · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage migration inhibitory factor (MIF) is a well-described proinflammatory mediator. MIF overexpression has been observed in many tumors and is implicated in oncogenic transformation and tumor progression. However, the molecular mechanisms responsible for regulating MIF expression remain poorly understood. In this study, we showed that the transcriptional repressor HBP1 (HMG box-containing protein 1) negatively regulates MIF expression. We first identified a large high-affinity HBP1 DNA-binding element at positions -811 to -792 from the transcriptional start site within the MIF promoter by computer analysis. Reporter analyses showed that this element was required for HBP1-mediated transcriptional repression. Furthermore, HBP1 associated with the MIF promoter in vivo and repressed endogenous MIF gene expression. Consistent with HBP1-mediated repression of MIF, low levels of HBP1 expression were associated with high levels of MIF expression in prostate cancer samples. Importantly, HBP1-mediated repression of MIF inhibited tumorigenic growth and invasion, and the repressive effect of HBP1 on tumorigenic growth and invasion could be partially rescued by the addition of recombinant MIF to the culture medium. Finally, prostate tumor samples with low HBP1 and high MIF expression were associated with a significant decrease in relapse-free survival. Taken together, these results indicated that HBP1 directly inhibited MIF gene transcription, and suggested that the loss of HBP1 expression or activity may contribute to the upregulation of MIF expression in prostate tumor tissue.
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