Department of Anesthesiology, The Eye, Ear, Nose and Throat Hospital of Fudan University, Shanghai Medical College of Fudan University, Shanghai, China.
Biomed Res Int. 2018 Apr 17;2018:8403157. doi: 10.1155/2018/8403157. eCollection 2018.
Lidocaine displays antitumor activity by inducing apoptosis and suppressing tumor growth in human hepatocellular carcinoma (HepG2) cells in vitro. However, the molecular mechanism underlying lidocaine-mediated antitumor activity is unclear. In this study, HepG2 cells were treated with lidocaine, and cell proliferation and colony-forming ability were assessed. The expression level of cytoplasmic polyadenylation element binding protein 3 was detected by real-time quantitative PCR and western blot. Lidocaine treatment resulted in decreased HepG2 cell viability and colony formation in a dose-dependent manner. In hepatocellular carcinoma patient samples, CPEB3 was downregulated and was associated with poor prognosis and high-grade malignancy. Additionally, CPEB3 was a critical mediator of lidocaine-induced repression of HepG2 cell proliferation. These results demonstrated that lidocaine decreased cell viability and colony-forming ability of HepG2 cells by upregulating CPEB3 expression.
利多卡因通过诱导细胞凋亡和抑制体外人肝癌（HepG2）细胞生长来发挥抗肿瘤活性。然而，利多卡因介导的抗肿瘤活性的分子机制尚不清楚。在这项研究中，用利多卡因处理 HepG2 细胞，并评估细胞增殖和集落形成能力。通过实时定量 PCR 和 Western blot 检测细胞质多聚腺苷酸化元件结合蛋白 3 的表达水平。利多卡因处理呈剂量依赖性降低 HepG2 细胞活力和集落形成。在肝细胞癌患者样本中，CPEB3 下调，与预后不良和高恶性度相关。此外，CPEB3 是利多卡因诱导的 HepG2 细胞增殖抑制的关键介质。这些结果表明，利多卡因通过上调 CPEB3 表达来降低 HepG2 细胞的活力和集落形成能力。
