Original Article
Copyright ©2013 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Sep 7, 2013; 19(33): 5485-5492
Published online Sep 7, 2013. doi: 10.3748/wjg.v19.i33.5485
Propofol induces apoptosis and increases gemcitabine sensitivity in pancreatic cancer cells in vitro by inhibition of nuclear factor-κB activity
Qi-Hang Du, Yan-Bing Xu, Meng-Yuan Zhang, Peng Yun, Chang-Yao He
Qi-Hang Du, Yan-Bing Xu, Meng-Yuan Zhang, Peng Yun, Chang-Yao He, Department of Anesthesiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong Province, China
Author contributions: Du QH and Xu YB contributed equally to the work. Du QH drafted the manuscript; Xu YB performed statistical analysis; Yun P, He CY and Zhang MY participated in the study design and coordination; all the authors have read and approved the final manuscript.
Correspondence to: Meng-Yuan Zhang, PhD, Department of Anesthesiology, Shandong Provincial Hospital Affiliated to Shandong University, 324 Jingwu Road, Jinan 250021, Shandong Province, China. duqihang@hotmail.com
Telephone: +86-531-68776472 Fax: +86-531-68776472
Received: February 16, 2013
Revised: April 3, 2013
Accepted: May 8, 2013
Published online: September 7, 2013
Core Tip

Core tip: Pretreatment of cells with propofol for 24 h followed by gemcitabine resulted in significant growth inhibition compared with gemcitabine alone. Overall growth inhibition correlated directly with apoptotic cell death. Propofol potentiated gemcitabine-induced killing by downregulation of nuclear factor-κB (NF-κB). In contrast, NF-κB was upregulated when pancreatic cancer cells were exposed to gemcitabine alone. These results suggested that inactivation of the NF-κB signaling pathway by propofol abrogated gemcitabine-induced activation of NF-κB resulting in the chemosensitization of pancreatic tumors to gemcitabine.