@Article{096504016X14823648620870,
AUTHOR = {Zhuang Kun, Guo Hanqing, Tang Hailing, Yan Yuan, Zhang Jun, Zhang Lingxia, Han Kun, Zhang Xin},
TITLE = {Gastrin Enhances Autophagy and Promotes Gastric Carcinoma  Proliferation via Inducing AMPKα},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {8},
PAGES = {1399--1407},
URL = {http://www.techscience.com/or/v25n8/56925},
ISSN = {1555-3906},
ABSTRACT = {Gastric cancer (GC) is one of the most frequent epithelial malignancies worldwide. The gastrointestinal (GI) 
peptide gastrin is an important regulator of the secretion and release of gastric acid from stomach parietal 
cells, and it also plays a vital role in the development and progression of GC. The aim of the current study 
was to investigate the role and underlying mechanism of gastrin and autophagy in regulating GC tumorigenesis. Gastrin-17 amide (G-17) was applied in the GC cell lines SGC7901 and MGC-803. The results showed 
that G-17 maintained the high viability of SGC7901 and MGC-803. The expression of autophagy marker 
proteins LC3II and Beclin1 was significantly increased, while the autophagy substrate p62 was obviously 
decreased in the gastrin group compared with the control group. Moreover, G-17 strengthened the expressions 
of AMPKα, Ras, Raf, MEK, and ERK1/2. Additionally, administration of AMPKα siRNA counteracted the 
effect of gastrin in SGC7901 cells. Finally, in an in vivo study of the tumor growth and survival rate of rats, the 
levels of AMPKα/Ras/Raf/MEK/ERK were significantly increased in the gastrin group and decreased following AMPKα shRNA injection. In conclusion, these findings indicate that gastrin plays a tumorigenic role by 
promoting autophagy in GC and may provide a novel therapeutic target for GC treatment.},
DOI = {10.3727/096504016X14823648620870}
}