ArticleWorld journal of clinical oncology2025
Role of cell cycle-related gene
Article in World journal of clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The trial behind it
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Who cites it
3 citing papers in PubMed.
- Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study.Frontiers in oncology · 2026Article
- Nitidine chloride inhibits colorectal cancer by targeting BUB1: mechanistic insights from molecular dynamics simulation, spatial transcriptomics, and single-cell RNA sequencing.BMC gastroenterology · 2025Article
- Article
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Authors and funding
13 authors.
Funding
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Abstract
backgroundHepatocellular carcinoma (HCC) is at the forefront of the global spectrum of cancer incidence and mortality, with conventional therapies like tyrosine kinase inhibitors limited by resistance. Recent studies have highlighted the promising anticancer effects of nitidine chloride (NC) against HCC. SAC3 domain containing 1 (SAC3D1) is critical for centrosome replication and spindle formation. However, research on SAC3D1 in HCC and NC remains limited.
aimTo investigate the mechanisms underlying SAC3D1's role in HCC progression and evaluated its potential as a therapeutic target of NC.
methodsRNA sequencing (RNA-seq) identified SAC3D1 expression changes in HCC cells after NC treatment. Molecular docking was further employed to validate the direct binding between NC and SAC3D1. Additionally, HCC multicenter data (The Cancer Genome Atlas_GTEx, ArrayExpress), pathway analysis, Pearson correlation analysis and SAC3D1
resultsRNA-seq showed that NC treatment significantly downregulated SAC3D1 expression [log
conclusionAs a potential target of NC, SAC3D1 may inhibit HCC progression through cell cycle regulation following its downregulation by NC.
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