ArticleCancer cell international2025
Kaempferol triggers cellular senescence via CDK1 ubiquitination in HCC cells.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
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Who cites it
1 citing paper in PubMed.
- The Implications of Radiotherapy-Induced Cellular Senescence for Cancer Treatment and Tumor Microenvironment Modulation.International journal of biological sciences · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
Hepatocellular carcinoma (HCC) is a common malignancy with poor prognosis. Cellular senescence, a state linked to cell cycle arrest, represents a potential therapeutic strategy for cancer. However, the clinical impact and regulatory mechanism of cellular senescence in HCC remains incompletely unknown. We identified HCC associated differentially expressed genes (DEGs) using bioinformatics analysis of public databases (TCGA, GEO, GEPIA, etc.). Enrichment, prognostic, risk scoring models analyses revealed cyclin-dependent kinase 1 (CDK1) as a core senescence-related gene. CDK1 expression was upregulated in HCC tissues and correlated with poor prognosis of HCC patients. In addition, CDK1 knockdown significantly increased senescence markers (the level or activity of P16, P21, and SA-β-gal), and induced cellular senescence in HepG2 cells. Molecular docking demonstrated high-affinity binding between CDK1 and kaempferol (KAE; affinity = -9.7 kcal/mol). KAE treatment similarly increased senescence markers and promoted cellular senescence in HepG2 cells. Mechanistically, KAE reduced CDK1 protein levels by promoting its ubiquitination and subsequent degradation. These findings indicated that KAE might induce cellular senescence through CDK1 ubiquitination, providing potential drugs and targets for HCC treatment.
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