@Article{096504019X15668125347026,
AUTHOR = {Yangmei Zhang, Xichang Zhou, Long Cheng, Xiang Wang, Qinglin Zhang, Youwei Zhang, Sanyuan Sun},
TITLE = {PRKAA1 Promotes Proliferation and Inhibits Apoptosis of Gastric Cancer Cells  Through Activating JNK1 and Akt Pathways},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {3},
PAGES = {213--223},
URL = {http://www.techscience.com/or/v28n3/48527},
ISSN = {1555-3906},
ABSTRACT = {PRKAA1 (protein kinase AMP-activated catalytic subunit 1) is a catalytic subunit of AMP-activated protein 
kinase (AMPK), which plays a key role in regulating cellular energy metabolism through phosphorylation, 
and genetic variations in the PRKAA1 have been found to be associated with gastric cancer risk. However, the 
effect and underlying molecular mechanism of PRKAA1 on gastric cancer tumorigenesis, especially the proliferation and apoptosis, are not fully understood. Our data showed that PRKAA1 is highly expressed in BGC-
823 and MKN45 cells and is expressed low in SGC-7901 and MGC-803 cells in comparison with the other 
gastric cancer cells. PRKAA1 downregulation by shRNA or treatment of AMPK inhibitor compound C significantly inhibited proliferation as well as promoted cell cycle arrest and apoptosis of BGC-823 and MKN45 cells. 
Moreover, the expression of PCNA and Bcl-2 and the activity of JNK1 and Akt signaling were also reduced 
in BGC-823 and MKN45 cells after PRKAA1 downregulation. In vivo experiments demonstrated that tumor 
growth in nude mice was significantly inhibited after PRKAA1 silencing. Importantly, inactivation of JNK1 
or Akt signaling pathway significantly inhibited PRKAA1 overexpression-induced increased cell proliferation 
and decreased cell apoptosis in MGC-803 cells. In conclusion, our findings suggest that PRKAA1 increases 
proliferation and restrains apoptosis of gastric cancer cells through activating JNK1 and Akt pathways.},
DOI = {10.3727/096504019X15668125347026}
}