UP-1.085: Changes of Prostate Cancer Cell Line DU145 in Migration and Invasion Capabilities after Down-Regulation of EF-1 Alpha Gene Expression

Urology ◽  
2009 ◽  
Vol 74 (4) ◽  
pp. S196-S197
Author(s):  
W. Yan ◽  
G. Zhu
2020 ◽  
Vol 22 (6) ◽  
pp. 5209-5218
Author(s):  
Wei Chen ◽  
Li‑Na He ◽  
Yong Liang ◽  
Xiang Zeng ◽  
Cui‑Ping Wu ◽  
...  

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Bianca Cioni ◽  
Anniek Zaalberg ◽  
Judy R. van Beijnum ◽  
Monique H. M. Melis ◽  
Johan van Burgsteden ◽  
...  

Abstract The androgen receptor (AR) is the master regulator of prostate cancer (PCa) development, and inhibition of AR signalling is the most effective PCa treatment. AR is expressed in PCa cells and also in the PCa-associated stroma, including infiltrating macrophages. Macrophages have a decisive function in PCa initiation and progression, but the role of AR in macrophages remains largely unexplored. Here, we show that AR signalling in the macrophage-like THP-1 cell line supports PCa cell line migration and invasion in culture via increased Triggering Receptor Expressed on Myeloid cells-1 (TREM-1) signalling and expression of its downstream cytokines. Moreover, AR signalling in THP-1 and monocyte-derived macrophages upregulates IL-10 and markers of tissue residency. In conclusion, our data suggest that AR signalling in macrophages may support PCa invasiveness, and blocking this process may constitute one mechanism of anti-androgen therapy.


2015 ◽  
Vol 42 (1) ◽  
pp. 18-22
Author(s):  
K. Todorova ◽  
S. Hayrabedyan

Summary Prostate cancer is one of the most common malignancies and the second leading cause of death from cancer in men. MicroRNAs are noncoding RNAs that have a role of post-transcriptional regulators. In this study we investigated how the tumour suppressor miR-15a modulates main transcription factors like cMYB and AR in androgen sensitive prostate cancer cell line LNCaP. The miR-15a inhibitor, mimic, and their negative controls were transfected into LNCaP cells. Real-time PCR analysis was performed in order to estimate the transcript levels of cMYB and AR. Flow cytometry analysis was performed to measure the protein levels of cMYB and AR. A Cell migration assay was done for cells transfected with miR-15a inhibitor and mimic. We found that cMYB is down-regulated and AR is up-regulated by miR-15a on the transcriptional and protein levels. By reconstituting miR-15a, we found that its down regulation in prostate cancer contributes to cMYB-induced cancer progression and reduced androgen receptivity. The ability of miR-15a to suppress cancer cell viability and migration is a very important phenomenon for understanding cancer heterogeneity in regard to adapted therapeutic approach development.


2010 ◽  
Vol 3 (1) ◽  
pp. 86-98 ◽  
Author(s):  
Suvarna Bhamre ◽  
Debashis Sahoo ◽  
Robert Tibshirani ◽  
David L. Dill ◽  
James D. Brooks

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