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  • Title: CDK1 bridges NF-κB and β-catenin signaling in response to H. pylori infection in gastric tumorigenesis.
    Author: Zhu S, Al-Mathkour M, Cao L, Khalafi S, Chen Z, Poveda J, Peng D, Lu H, Soutto M, Hu T, McDonald OG, Zaika A, El-Rifai W.
    Journal: Cell Rep; 2023 Jan 31; 42(1):112005. PubMed ID: 36681899.
    Abstract:
    Infection with Helicobacter pylori (H. pylori) is the main risk factor for gastric cancer, a leading cause of cancer-related death worldwide. The oncogenic functions of cyclin-dependent kinase 1 (CDK1) are not fully understood in gastric tumorigenesis. Using public datasets, quantitative real-time PCR, western blot, and immunohistochemical (IHC) analyses, we detect high levels of CDK1 in human and mouse gastric tumors. H. pylori infection induces activation of nuclear factor κB (NF-κB) with a significant increase in CDK1 in in vitro and in vivo models (p < 0.01). We confirm active NF-κB binding sites on the CDK1 promoter sequence. CDK1 phosphorylates and inhibits GSK-3β activity through direct binding with subsequent accumulation and activation of β-catenin. CDK1 silencing or pharmacologic inhibition reverses these effects and impairs tumor organoids and spheroid formation. IHC analysis demonstrates a positive correlation between CDK1 and β-catenin. The results demonstrate a mechanistic link between infection, inflammation, and gastric tumorigenesis where CDK1 plays a critical role.
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