scholarly journals Leupaxin stimulates adhesion and migration of prostate cancer cells through modulation of the phosphorylation status of the actin-binding protein caldesmon

Oncotarget ◽  
2015 ◽  
Vol 6 (15) ◽  
pp. 13591-13606 ◽  
Author(s):  
Sascha Dierks ◽  
Sandra von Hardenberg ◽  
Thomas Schmidt ◽  
Felix Bremmer ◽  
Peter Burfeind ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Actin Binding ◽  
Prostate Cancer Cells ◽  
Actin Binding Protein ◽  
And Migration

NOL8, the binding protein for beta-catenin, promoted the growth and migration of prostate cancer cells

2018 ◽  
Vol 294 ◽  
pp. 40-47 ◽  
Author(s):  
Shuo Gu ◽  
Peijin Hou ◽  
Kun Liu ◽  
Xiaobing Niu ◽  
Bingjian Wei ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Beta Catenin ◽  
Prostate Cancer Cells ◽  
And Migration

DLX1, a binding protein of beta-catenin, promoted the growth and migration of prostate cancer cells

2018 ◽  
Vol 363 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Ming Liang ◽  
Yan Sun ◽  
Huai-Liang Yang ◽  
Bin Zhang ◽  
Ji Wen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Beta Catenin ◽  
Prostate Cancer Cells ◽  
And Migration

SWAP70, actin-binding protein, function as an oncogene targeting tumor-suppressive miR-145 in prostate cancer

The Prostate ◽  
2011 ◽  
Vol 71 (14) ◽  
pp. 1559-1567 ◽  
Author(s):  
Takeshi Chiyomaru ◽  
Shuichi Tatarano ◽  
Kazumori Kawakami ◽  
Hideki Enokida ◽  
Hirofumi Yoshino ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Function ◽  
Binding Protein ◽  
Actin Binding ◽  
Actin Binding Protein

scholarly journals Silencing of BACH1 inhibits invasion and migration of prostate cancer cells by altering metastasis-related gene expression

2017 ◽  
Vol 46 (7) ◽  
pp. 1495-1504 ◽  
Author(s):  
Neda Shajari ◽  
Sadaf Davudian ◽  
Tohid Kazemi ◽  
Behzad Mansoori ◽  
Shima Salehi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Cancer Cells ◽  
Related Gene ◽  
Prostate Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Silencing of ELK3 Induces S-M Phase Arrest and Apoptosis and Upregulates SERPINE1 Expression Reducing Migration in Prostate Cancer Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Yuanshen Mao ◽  
Wenfeng Li ◽  
Bao Hua ◽  
Xin Gu ◽  
Weixin Pan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Prostate Cancer Cells ◽  
Migration Inhibition ◽  
Akt Inhibitor ◽  
Phase Arrest ◽  
M Phase ◽  
And Migration

ELK3, an ETS domain-containing transcription factor, participates in various physiological and pathological processes including cell proliferation, migration, angiogenesis, and malignant progression. However, the role of ELK3 in prostate cancer cells and its mechanism are not fully understood. The contribution of ELK3 to prostate cancer progression was investigated in the present study. We showed that silencing of ELK3 by siRNA in prostate cancer cell DU145 induced S-M phase arrest, promoted apoptosis, inhibited cell proliferation and migration in vitro, and suppressed xenograft growth in mice in vivo. In accordance with its ability to arrest cells in S-M phase, the expression of cyclin A and cyclin B was downregulated. In addition, the expression of p53 was upregulated following ELK3 knockdown, while that of antiapoptotic Bcl-2 was decreased. The migration inhibition may partly due to upregulation of SERPINE1 (a serine protease inhibitor) followed ELK3 knockdown. Consistently, downregulation of SERPINE1 resulted in a modest elimination of migration inhibition resulted from ELK3 knockdown. Furthermore, we found that the AKT signaling was activated in ELK3 knockdown cells, and treatment these cells with AKT inhibitor attenuated SERPINE1 expression induced by ELK3 silencing, suggesting that activation of AKT pathway may be one of the reasons for upregulation of SERPINE1 after ELK3 knockdown. In conclusion, modulation of ELK3 expression may control the progression of prostate cancer partly by regulating cell growth, apoptosis, and migration.

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