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Pancreatic Neoplasms: HELP
Articles by Guo Wei
Based on 1 article published since 2010
(Why 1 article?)
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Between 2010 and 2020, Guo Wei wrote the following article about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Homoharringtonine could induce quick protein synthesis of PSMD11 through activating MEK1/ERK1/2 signaling pathway in pancreatic cancer cells. 2018

Wang, Lele / Zhao, Linlin / Wei, Guo / Saur, Dieter / Seidler, Barbara / Wang, Junyan / Wang, Chuanxin / Qi, Tonggang. ·Central Research Laboratory, The Second Hospital of Shandong University, Jinan, China. · Department of Dermatology, The Second Hospital of Shandong University, Jinan, China. · The II. Medizinische Klinik und Poliklinik der Technischen Universität München, München, Germany. · Department of Internal Medicine, Dezhou People's Hospital, Dezhou, China. · The Third People's Hospital of Tibet, Central Laboratory, Lhasa, China. ·J Cell Biochem · Pubmed #29665121.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) remains one of the most devastating disease with the 5-year survival rate less than 6%. In this study, we investigated if inhibiting protein synthesis directly with homoharringtonine (HHT) could induce acute apoptosis in pancreatic cancer cells through quick depletion of multiple short-lived critical members of the central proteome, example, PSMD11(26S proteasome non-ATPase regulatory subunit 11). It was shown that although HHT could inhibit proliferation and growth of MiaPaCa-2 and PANC-1 cells in a time- and dose-dependent manner, only part of pancreatic cancer cells could be induced to die through acute apoptosis. Mechanistic studies showed that HHT could induce quick protein synthesis of PSMD11 through activating MEK1/ERK1/2 signaling pathway in pancreatic cancer cells. Inhibiting MEK1/ERK1/2 pathway with sorafenib could improve the cytotoxity of HHT in vitro and in a genetically engineered mouse model of pancreatic cancer. These results suggest that quick induction of PSMD11 or other acute apoptosis inhibitors through activation of the MEK1/ERK1/2 signaling pathway may be one of the important surviving mechanism which can help pancreatic cancer cells avoid acute apoptosis, it may have significant implications for the targeted therapy of pancreatic ductal adenocarcinoma.