International Journal Of Bilogical Sciences
.: Home > International Journal Of Bilogical Sciences > 2012 > Volume 8 Number 1 > Wei-Tian Wei2,3,#, Hui Chen3, #, Zhao-Hong Wang3, Zhong-Lin Ni3, Hai-Bin Liu3, Hong-Fei Tong3, Hong-Chun Guo3, Dian-Lei Liu3, Sheng-Zhang Lin1,3,✉
Enhanced Antitumor Efficacy of Gemcitabine by Evodiamine on Pancreatic Cancer via Regulating PI3K/Akt Pathway
Wei-Tian Wei2,3,#, Hui Chen3, #, Zhao-Hong Wang3, Zhong-Lin Ni3, Hai-Bin Liu3, Hong-Fei Tong3, Hong-Chun Guo3, Dian-Lei Liu3, Sheng-Zhang Lin1,3,✉
1. Department of Hepato-biliary-pancreatic Surgery, First Affiliated Hospital of Medical College, Zhejiang University, Hangzhou, China. 2. Department of Oncological Surgery, Zhejiang Cancer Hospital, Hangzhou, China. 3. Department of Hepato-biliary-pancreatic Surgery, Second Affiliated Hospital of Wenzhou Medical College, Zhejiang, China.
Evodiamine has therapeutic potential against cancers. This study was designed to investigate whether combination therapy with gemcitabine and evodiamine enhanced antitumor efficacy in pancreatic cancer. In vitro application of the combination therapy triggered significantly higher frequency of pancreatic cancer cells apoptosis, inhibited the activities of PI3K, Akt, PKA, mTOR and PTEN, and decreased the activation of NF-κB and expression of NF-κB-regulated products. In vivo application of the combination therapy induced significant enhancement of tumor cell apoptosis, reductions in tumor volume, and inhibited activation of mTOR and PTEN. In conclusion, evodiamine can augment the therapeutic effect of gemcitabine in pancreatic cancer through direct or indirect negative regulation of the PI3K/Akt pathway.
evodiamine, gemcitabine, pancreatic cancer SW1990 cells, apoptosis, PTEN, mTOR
Date Deposited : 08 Apr 2015 13:50
Official URL: http://www.ijbs.com/ms/archive
Last Modified : 08 Apr 2015 13:50
Volume 8, Number 1, - 2012 , ISSN 1545-1003
Full Text Original