PKG II Inhibits EGF/EGFR-Induced Migration of Gastric Cancer Cells

• DOI: 10.1371/journal.pone.0061674
• Publication Date: 2013-04-16T16:58:50Z
• Authors: Lu Jiang; Ting Lan; Yongchang Chen; Jianrong Sang; Yueying Li; Min Wu; Yan Tao; Ying Wang; Hai Qian; Luo Gu
• Keywords: 0301 basic medicine; Epidermal Growth Factor; Science; Q; R; Cyclic GMP-Dependent Protein Kinase Type II; Thionucleotides; Cell Line; 3. Good health; ErbB Receptors; 03 medical and health sciences; Cell Movement; Stomach Neoplasms; Cell Line, Tumor; Medicine; Humans; Phosphorylation; Cyclic GMP; Research Article; Signal Transduction

Background Our previous research results showed that Type II cGMP dependent protein kinase (PKG II) could block the activation of epidermal growth factor receptor (EGFR) and consequently inhibit proliferation related MAPK/ERK-mediated signal transduction gastric cancer cell line BGC-823, suggesting PKG might other EGFR-triggered pathways biological activities cells. This paper was designed to investigate potential inhibition on EGF/EGFR-induced migration activity pathways. Methodology/Principal Findings In AGS, expression were increased by infecting cells with adenoviral construct encoding cDNA (Ad-PKG treating analogue 8-pCPT-cGMP. Phosphorylation proteins detected Western Blotting active small G Ras Rac1 measured "Pull-down" method. Cell trans-well equipment. Binding between EGFR Co-IP. The EGF stimulated AGS effect PLCγ1 ERK-mediated inhibited EGF-induced blocked EGF-initiated through preventing Tyr 992 1068 phosphorylation EGFR. bound caused threonine it. Conclusion/Significance systemically confirms pathways, indicating has a fargoing EGF/EGFR phosphorylating blocking