ArticleCell biology and toxicology2025
MCM8 promotes NR4A1-mediated E2F1 transcription and facilitates renal cell carcinoma through enhancing aerobic glycolysis.
Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Targeting the nuclear orphan receptor NR4A1: a key target in lung cancer progression and therapeutic resistance.Frontiers in oncology · 2025Review
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7 authors.
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Abstract
Renal cell carcinoma (RCC) is a type of renal malignancy originated from the urinary tubular epithelial system. Despite its high incidence, the molecular mechanisms driving its pathogenesis remain poorly understood, limiting therapeutic advancements. This study explored the link between MCM8 and RCC progression. MCM8 displays significantly high expression in RCC tissues and was closely associated with RCC pathological staging. Knocking down endogenous MCM8 in RCC cells significantly suppressed malignant phenotypes, while simultaneously inducing apoptosis. Similarly, in vivo experiments confirmed these findings, showing a pronounced reduction in tumor growth upon MCM8 silencing. Mechanistic investigations revealed that MCM8 regulates E2F1 expression by interacting with the transcription factor NR4A1, thereby affecting E2F1 transcriptional activity. Additionally, MCM8 and E2F1 collaboratively influence aerobic glycolysis and the cellular behavior of RCC cells. In conclusion, this study identifies MCM8 as a tumor-promoting factor in RCC, with its oncogenic role potentially mediated by its regulation of E2F1 expression.
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