scholarly journals Inhibition of epithelial to mesenchymal transition in metastatic prostate cancer cells by the novel proteasome inhibitor, NPI-0052: pivotal roles of Snail repression and RKIP induction

Oncogene ◽  
2009 ◽  
Vol 28 (40) ◽  
pp. 3573-3585 ◽  
Author(s):  
S Baritaki ◽  
A Chapman ◽  
K Yeung ◽  
D A Spandidos ◽  
M Palladino ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Proteasome Inhibitor ◽  
Metastatic Prostate Cancer ◽  
Epithelial To Mesenchymal Transition ◽  
The Novel ◽  
Prostate Cancer Cells ◽  
Mesenchymal Transition

Abstract 1124: ETS1 regulates epithelial-to-mesenchymal transition (EMT) in prostate cancer cells

2014 ◽  
Author(s):  
Jamie J. Rodgers ◽  
Michael Epis ◽  
Ronald Cohen ◽  
Peter Leedman ◽  
Jennet Harvey ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Prostate Cancer Cells ◽  
Mesenchymal Transition

scholarly journals Cholesterol Induces Epithelial-to-Mesenchymal Transition of Prostate Cancer Cells by Suppressing Degradation of EGFR through APMAP

2019 ◽  
Vol 79 (12) ◽  
pp. 3063-3075 ◽  
Author(s):  
Siyuan Jiang ◽  
Xuetong Wang ◽  
Dalong Song ◽  
XiaoJun Liu ◽  
Yinmin Gu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Prostate Cancer Cells ◽  
Mesenchymal Transition

scholarly journals Glycidamide Promotes the Growth and Migratory Ability of Prostate Cancer Cells by Changing the Protein Expression of Cell Cycle Regulators and Epithelial-to-Mesenchymal Transition (EMT)-Associated Proteins with Prognostic Relevance

2019 ◽  
Vol 20 (9) ◽  
pp. 2199
Author(s):  
Titus Ime Ekanem ◽  
Chi-Chen Huang ◽  
Ming-Heng Wu ◽  
Ding-Yen Lin ◽  
Wen-Fu T. Lai ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Protein Expression ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Epithelial To Mesenchymal Transition ◽  
Gene Signature ◽  
Prostate Cancer Cells ◽  
Mesenchymal Transition ◽  
Prognostic Relevance

Acrylamide (AA) and glycidamide (GA) can be produced in carbohydrate-rich food when heated at a high temperature, which can induce a malignant transformation. It has been demonstrated that GA is more mutagenic than AA. It has been shown that the proliferation rate of some cancer cells are increased by treatment with GA; however, the exact genes that are induced by GA in most cancer cells are not clear. In the present study, we demonstrated that GA promotes the growth of prostate cancer cells through induced protein expression of the cell cycle regulator. In addition, we also found that GA promoted the migratory ability of prostate cancer cells through induced epithelial-to-mesenchymal transition (EMT)-associated protein expression. In order to understand the potential prognostic relevance of GA-mediated regulators of the cell cycle and EMT, we present a three-gene signature to evaluate the prognosis of prostate cancer patients. Further investigations suggested that the three-gene signature (CDK4, TWIST1 and SNAI2) predicted the chances of survival better than any of the three genes alone for the first time. In conclusion, we suggested that the three-gene signature model can act as marker of GA exposure. Hence, this multi-gene panel may serve as a promising outcome predictor and potential therapeutic target in prostate cancer patients.

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