Procyanidins from Cinnamomi Cortex promote proteasome-independent degradation of nuclear Nrf2 through phosphorylation of insulin-like growth factor-1 receptor in A549 cells

2017 ◽  
Vol 635 ◽  
pp. 66-73 ◽  
Author(s):  
Tomokazu Ohnuma ◽  
Kazuya Sakamoto ◽  
Asumi Shinoda ◽  
Chiaki Takagi ◽  
Shoko Ohno ◽  
...  
Keyword(s):  
Growth Factor ◽  
A549 Cells ◽  
Insulin Like Growth Factor ◽  
Cinnamomi Cortex

scholarly journals Silencing of the type 1 insulin-like growth factor receptor increases the sensitivity to apoptosis and inhibits invasion in human lung adenocarcinoma A549 cells

2007 ◽  
Vol 12 (4) ◽  
Author(s):  
Zhiyuan Ma ◽  
Aiqiang Dong ◽  
Minjian Kong ◽  
Jianfang Qian
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Human Lung ◽  
A549 Cells ◽  
Growth Factor Receptor ◽  
Insulin Like Growth Factor ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

AbstractThe type 1 insulin-like growth factor receptor (IGF-1R), which is over-expressed or activated in many human cancers, including lung cancer, mediates cancer cell proliferation and metastasis. Several studies indicate that blocking IGF-1R expression can inhibit tumor cell proliferation and metastasis. In this study, inhibition of the endogenous IGF-1R by recombinant adenoviruses encoding short hairpin RNAs against IGF-1R was found to significantly suppress IGF-1R expression, arrest the cell cycle, enhance the apoptotic response, and inhibit proliferation, adhesion, invasion and migration in A549 cells. Moreover, silencing IGF-1R decreases the expression of invasive-related genes including matrix metalloproteinase-2 (MMP-2), MMP-9, and urokinase-plasminogen activator (u-PA), and the phosphorylation of Akt and ERK1/2. These results suggest that the silencing of IGF-1R has the potential to be an effective cancer gene therapy strategy for human lung cancer.

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