Association NEDD9 with TGF-β-triggered epithelial-mesenchymal transition and cell invasion in prostate cancer cells: implications for cancer aggressiveness

2014 ◽  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Prostate Cancer Cells ◽  
Mesenchymal Transition ◽  
Cancer Aggressiveness

NEDD9 crucially regulates TGF-β-triggered epithelial-mesenchymal transition and cell invasion in prostate cancer cells: Involvement in cancer progressiveness

The Prostate ◽  
2014 ◽  
Vol 74 (8) ◽  
pp. 901-910 ◽  
Author(s):  
Kazuya Morimoto ◽  
Tomoaki Tanaka ◽  
Yujiro Nitta ◽  
Keiko Ohnishi ◽  
Hidenori Kawashima ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Prostate Cancer Cells ◽  
Mesenchymal Transition

scholarly journals Periostin Mediates TGF-β-Induced Epithelial Mesenchymal Transition in Prostate Cancer Cells

2015 ◽  
Vol 36 (2) ◽  
pp. 799-809 ◽  
Author(s):  
Qingfeng Hu ◽  
Shijun Tong ◽  
Xiaojun Zhao ◽  
Weihong Ding ◽  
Yuancheng Gou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Associated Factors ◽  
Epithelial Mesenchymal Transition ◽  
Prostate Cancer Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Background: In our previous study, we found that periostin was upregulated in prostate cancer, and its expression could be modulated by TGF-β. TGF-β could upregulate periostin expression in some cells, and both TGF-β and periostin could induce epithelial mesenchymal transition (EMT). We aimed to study the effect of periostin in the process of TGF-β-induced EMT in prostate cancer cells. Methods: We constructed a lentivirus vector containing the periostin gene and transduced it into PC3 and DU145 cells. After confirming periostin overexpression by PCR and Western blotting, we used an MTT assay to establish a growth curve to measure cell proliferation. Additionally, we performed transwell and wound healing assays to measure cell invasion and migration, respectively. Lastly, we measured the expression of EMT associated factors using Western blot analysis to test the effect of periostin on EMT in prostate cancer cells. Results: PCR and Western blot analyses confirmed that periostin was upregulated after infection with the periostin lentiviral vector. Periostin overexpression promoted increased cell proliferation, invasion, and migration as measured by MTT, transwell, and wound healing assays, respectively. Western blot analysis illustrated that periostin overexpression increased the expression of EMT associated factors, and periostin overexpression activated Akt and GSK-3β, which could be inhibited using a PI3K inhibitor. Additionally, TGF-β increased the levels of STAT3, Twist1 and periostin, while both STAT3 shRNA and Twist1 shRNA inhibited periostin expression. However, STAT3 shRNA also decreased Twist1 expression. Although reduction of STAT3, Twist1 or periostin levels with shRNA inhibited TGF-β-induced overexpression of EMT associated factors, periostin overexpression could reverse such inhibition by interfering with STAT3 and Twist1. Similarly, periostin overexpression also reversed inhibition of cell invasion induced by interference of STAT3 and Twist1. Conclusion: Our findings indicate that periostin is an important mediator of TGF-β-induced EMT and suggest that periostin is a potential therapeutic target for suppressing the metastatic progression of prostate cancer.

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