Identification of CDK1 as a Biomarker for the Treatment of Liver Fibrosis and Hepatocellular Carcinoma Through Bioinformatics Analysis

Cyclin-dependent kinase 1 (CDK1) has emerged as a critical regulator of cell cycle progression, yet its role in liver fibrosis-associated hepatocellular carcinoma (LF-HCC) remains underexplored. This study aimed to systematically evaluate CDK1's prognostic significance, immune regulatory functions, and therapeutic potential in LF-HCC pathogenesis. Integrated bioinformatics approaches were applied to multi-omics datasets from GEO, TCGA, and TIMER databases. Differentially expressed genes were identified through enrichment analysis and protein-protein interaction networks. Survival outcomes were assessed via Kaplan-Meier analysis, while immune cell infiltration patterns were quantified using CIBERSORT. Molecular docking simulations evaluated CDK1's binding affinity with pharmacologically active compounds (alvocidib, seliciclib, alsterpaullone) using AutoDock Vina. CDK1 demonstrated significant overexpression in LF-HCC tissues compared to normal controls (<i>p</i> < 0.001). Elevated CDK1 expression correlated with reduced overall survival (HR = 2.41, 95% CI:1.78-3.26, <i>p</i> = 0.003) and advanced tumor staging (<i>p</i> = 0.007). Immune profiling revealed strong associations between CDK1 levels and immunosuppressive cell infiltration, particularly regulatory T cells (r = 0.63, <i>p</i> = 0.001) and myeloid-derived suppressor cells (r = 0.58, <i>p</i> = 0.004). Molecular docking confirmed high-affinity binding of CDK1 to kinase inhibitors through conserved hydrogen-bond interactions (binding energy ≤ -8.5 kcal/mol), with alvocidib showing optimal binding stability. This multimodal analysis establishes CDK1 as both a prognostic biomarker and immunomodulatory regulator in LF-HCC pathogenesis. The enzyme's dual role in driving tumor progression and reshaping the immune microenvironment positions it as a promising therapeutic target. Computational validation of CDK1 inhibitors provides a rational basis for developing precision therapies against LF-HCC, bridging translational gaps between biomarker discovery and clinical application.