ArticleBMC cancer2022
Functional interaction between S100A1 and MDM2 may modulate p53 signaling in normal and malignant endometrial cells.
Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Differential Expression of S100A8 in Tumor and Immune Compartments of Endometrial Carcinoma and Its Clinical Relevance.Medicina (Kaunas, Lithuania) · 2025Article
- Role of Extracellular Vesicles in TSC Renal Cystogenesis.International journal of molecular sciences · 2025Article
- Advances in S100 protein family for gynecological malignancies.Discover oncology · 2025Review
- Observational
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundS100A1 expression is deregulated in a variety of human malignancies, but its role in normal and malignant endometrial cells is unclear.
methodsWe used endometrial carcinoma (Em Ca) cell lines to evaluate the physical and functional interaction of S100A1 with p53 and its negative regulator, mouse double minute 2 (MDM2). We also evaluated the expression of S100A1, p53, and MDM2 in clinical samples consisting of 89 normal endometrial and 189 Em Ca tissues.
resultsS100A1 interacted with MDM2 but not p53 in Em Ca cell lines. Treatment of cells stably overexpressing S100A1 with Nutlin-3A, an inhibitor of the p53/MDM2 interaction, increased expression of p53-target genes including p21
conclusionThe interaction between S100A1 and MDM2 may modulate proliferation, susceptibility to apoptosis, and migration through alterations in p53 signaling in normal- but not malignant-endometrial cells.
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