Effects of Lidocaine-Mediated CPEB3 Upregulation in Human Hepatocellular Carcinoma Cell Proliferation In Vitro.

Hongjun Liu,Wenxian Li,Yiru Wang,Xia Shen,Bing Chen

doi:10.1155/2018/8403157

Abstract

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 (CPEB3) 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.

Highlights

Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world and is associated with poor patient prognosis [1]
Recent studies have demonstrated that anesthetics exerted antitumor effects by suppressing cell proliferation, inducing apoptosis, and by inhibiting cell migration [9, 10, 20,21,22]
Lidocaine has been shown to induce apoptosis of breast tumor cells when treated with concentrations similar to those used clinically [20]

Summary

Introduction

Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world and is associated with poor patient prognosis [1]. According to the latest Global Cancer Statistics, HCC is the fifth most prevalent cancer in men and the ninth most prevalent cancer in women. Surgery remains an important treatment option for HCC [3]. Other complicating factors (e.g., perioperative care and anesthetic management) may influence disease progression and recurrence [4, 5]. Several retrospective studies have reported that regional anesthesia, epidural analgesia, and perioperative analgesia could influence disease-free survival outcomes for cancer patients [6,7,8]. Previous studies have demonstrated that lidocaine effectively inhibited the proliferation and invasion of tumor cells and that lidocaine use was associated with improved disease-free survival outcomes for cancer patients after surgery [9,10,11,12,13]. The molecular mechanisms underlying this improved patient outcome remain unknown

Methods

Results

Conclusion