ArticleBMC molecular biology2012
Transcriptional activation of microRNA-34a by NF-kappa B in human esophageal cancer cells.
Article in BMC molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 98 citations in OpenAlex.
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- ESOMIR: a curated database of biomarker genes and miRNAs associated with esophageal cancer.Database : the journal of biological databases and curation · 2023Article
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- CORM-A1 Alleviates Pro-Atherogenic Manifestations via miR-34a-5p Downregulation and an Improved Mitochondrial Function.Antioxidants (Basel, Switzerland) · 2023Article
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- Role of microRNA-34a in blood-brain barrier permeability and mitochondrial function in ischemic stroke.Frontiers in cellular neuroscience · 2023Review
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- Altered expression of miR-29a-3p and miR-34a-5p by specific inhibition of GSK3β in the MPPNon-coding RNA research · 2022Article
- Bile reflux and hypopharyngeal cancer (Review).Oncology reports · 2021Review
- The comprehensive landscape of miR-34a in cancer research.Cancer metastasis reviews · 2021Review
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- The temporal effects of topical NF-Oncotarget · 2020Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundmiR-34a functions as an important tumor suppressor during the process of carcinogenesis. However, the mechanism of miR-34a dysregulation in human malignancies has not been well elucidated. Our study aimed to further investigate the regulation mechanism of miR-34a.
resultsWe found that overexpression of NF-kappa B p65 subunit could increase miR-34a levels in EC109, an esophageal squamous cancer cell line, while ectopic expression of DN IkappaB leaded to a significant reduction of miR-34a expression. Bioinformatics analysis suggested three putative KB sites in promoter region of miR-34a gene. Mutation two of these KB sites impaired p65 induced miR-34a transcriptional activity. Chromatin immunoprecipitation and electrophoretic mobility shift assays both showed that NF-kappaB could specifically bind to the third KB site located in miR-34a promoter. In addition, we found that overexpression of NF-kappaB p65 could not successfully induce miR-34a expression in esophageal cancer cell lines with mutant p53 or decreased p53. Reporter assay further showed that NF-kappaB-induced miR-34a transcriptional activity was reduced by p53 impairment. Nevertheless, CHIP analysis suggested binding of NF-kappaB to miR-34a promoter was not affected in cells with mutant p53.
conclusionsOur work indicates a novel mechanism of miR-34a regulation that NF-kappaB could elevate miR-34a expression levels through directly binding to its promoter. And wildtype p53 is responsible for NF-kappaB-mediated miR-34a transcriptional activity but not for NF-kappaB binding. These findings might be helpful in understanding miR-34a abnormality in human malignancies and open new perspectives for the roles of miR-34a and NF-kappaB in tumor progression.
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