ArticleOncology letters2018
MED28 increases the colony-forming ability of breast cancer cells by stabilizing the ZNF224 protein upon DNA damage.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
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
7 citing papers in PubMed, 10 citations in OpenAlex.
- ZNF224 enhances the oncogenic function of p21 via p53 and AKT pathways in melanoma.The FEBS journal · 2025Article
- ZNF224 Protein: Multifaceted Functions Based on Its Molecular Partners.Molecules (Basel, Switzerland) · 2021Review
- Article
- Comprehensive Transcriptome Analysis Reveals Insights into Phylogeny and Positively Selected Genes ofAnimals : an open access journal from MDPI · 2020Article
- MED28 Over-Expression Shortens the Cell Cycle and Induces Genomic Instability.International journal of molecular sciences · 2019Article
- The clinicopathological significance of ZNF10 in invasive ductal carcinoma of the breast.International journal of clinical and experimental pathology · 2018Article
- A multiple genomic data fused SF2 prediction model, signature identification, and gene regulatory network inference for personalized radiotherapy.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regulation of gene expression by transcription factors serves a critical function in cell proliferation. Zinc-finger protein 224 (ZNF224), a Krüppel-associated-box-containing zinc finger protein, is known to serve a crucial function in integrating the transcriptional co-factors that activate transcriptional regulation pathways in the cell. A previous study demonstrated that ZNF224 enhances cell proliferation by downregulating the expression of p21 and p53. The present study identified mediator complex subunit 28 (MED28) as a potential binding partner for ZNF224; this was confirmed by co-immunoprecipitation and a surface plasmon resonance assay. Additionally, the KRAB domain at the N-terminal of ZNF224 interacts with the MED domain of MED28. Bimolecular fluorescence complementation analysis revealed that ZNF224 associates with MED28 in the nucleus. In addition, ZNF224 was rapidly degraded upon treatment with the DNA-damaging agent camptothecin (CPT). Transient overexpression of MED28 inhibited the CPT-mediated degradation of ZNF224, resulting in increased colony formation by MCF-7 cells. The molecular mechanisms that underlie the biological outcomes of MED28 expression have not yet been fully elucidated. The present study provides molecular evidence for the function of ZNF224 and MED28 in the DNA-damage response.
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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.