Abstract：
Interventional chemotherapy is a common operation in the clinical treatment of liver cancer. The aim of this study was to investigate the expression and molecular mechanism of serum miR-4746-5p in liver cancer patients before and after interventional chemotherapy. The levels of miR-4746-5p and CDKN1C in serum samples from liver cancer patients were detected using real-time fluorescence quantitative polymerase chain reaction. Receiver operating characteristic curves revealed the diagnostic value of miR-4746-5p in tumors. Differences in clinical indicators between liver cancer patients and healthy controls were assessed using Pearson correlation analysis. Luciferase reporter gene assays confirmed the targeted interaction between miR-4746-5p and CDKN1C. In vitro cellular assays were validated by Cell Counting Kit-8, Transwell assay, and chemoresistance assay. Serum miR-4746-5p levels were increased in liver cancer patients but were downregulated after chemotherapy intervention. CDKN1C expression showed the opposite trend. Low levels of miR-4746-5p mediated cell growth and metastasis by targeting and negatively regulating CDKN1C expression, while silencing CDKN1C restored cell activity. Inhibition of miR-4746-5p reduced chemoresistance, while downregulation of CDKN1C affected cell sensitivity. miR-4746-5p may be a potential therapeutic factor for liver cancer diagnosis and interventional chemotherapy.
摘要：
介入化疗是肝癌临床治疗中常见的手术方式。本研究旨在探讨肝癌患者介入化疗前后血清miR-4746-5p的表达及其分子机制。采用实时荧光定量聚合酶链反应检测肝癌患者血清中miR-4746-5p和CDKN1C水平。受试者工作特征曲线揭示miR-4746-5p在肿瘤中的诊断价值。使用Pearson相关性分析评估肝癌患者和健康对照组之间临床指标的差异。荧光素酶报告基因测定证实了miR-4746-5p和CDKN1C之间的靶向相互作用。体外细胞测定通过细胞计数试剂盒-8，Transwell测定，和化学抗性测定。肝癌患者血清miR-4746-5p水平升高，但在化疗干预后下调。CDKN1C表达呈相反趋向。低水平的miR-4746-5p通过靶向和负调控CDKN1C表达介导细胞生长和转移，而沉默CDKN1C恢复细胞活性。抑制miR-4746-5p降低化学抗性，而CDKN1C下调影响细胞敏感性。miR-4746-5p可能是肝癌诊断和介入化疗的潜在治疗因子。
