Activation of AMP-activated protein kinase on human gastric cancer cells by apoptosis induced by corosolic acid isolated from Weigela subsessilis

2010 ◽  
Vol 24 (12) ◽  
pp. 1857-1861 ◽  
Author(s):  
Myung Sun Lee ◽  
Chang Min Lee ◽  
Eun Young Cha ◽  
Phuong Thien Thuong ◽  
KiHwan Bae ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Corosolic Acid ◽  
Weigela Subsessilis ◽  
Amp Activated Protein Kinase

Adenosine induces apoptosis in the human gastric cancer cells via an intrinsic pathway relevant to activation of AMP-activated protein kinase

2004 ◽  
Vol 67 (10) ◽  
pp. 2005-2011 ◽  
Author(s):  
Masaru Saitoh ◽  
Kaoru Nagai ◽  
Kazuhiko Nakagawa ◽  
Takehira Yamamura ◽  
Satoshi Yamamoto ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Intrinsic Pathway ◽  
Gastric Cancer Cells ◽  
Amp Activated Protein Kinase

scholarly journals PRKAA1 Promotes Proliferation and Inhibits Apoptosis of Gastric Cancer Cells Through Activating JNK1 and Akt Pathways

2020 ◽  
Vol 28 (3) ◽  
pp. 213-223 ◽  
Author(s):  
Yangmei Zhang ◽  
Xichang Zhou ◽  
Long Cheng ◽  
Xiang Wang ◽  
Qinglin Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Akt Signaling ◽  
Catalytic Subunit ◽  
Gastric Cancer Cells ◽  
In Vivo Experiments ◽  
Compound C ◽  
Amp Activated Protein Kinase

PRKAA1 (protein kinase AMP-activated catalytic subunit α 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.

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