Overexpression of 5α-reductase type 1 increases sensitivity of prostate cancer cells to low concentrations of testosterone

The Prostate ◽  
2009 ◽  
Vol 69 (6) ◽  
pp. 595-602 ◽  
Author(s):  
Lynn N. Thomas ◽  
Robert C. Douglas ◽  
Roger S. Rittmaster ◽  
Catherine K.L. Too
2013 ◽  
Vol 4 ◽  
pp. 739-744 ◽  
Author(s):  
Agnieszka Wanda Piastowska-Ciesielska ◽  
Marcin Kozłowski ◽  
Waldemar Wagner ◽  
Kamila Domińska ◽  
Tomasz Ochędalski

2013 ◽  
Vol 94 (3) ◽  
pp. 458-465 ◽  
Author(s):  
Albert Hagelgans ◽  
Mario Menschikowski ◽  
Susanne Fuessel ◽  
Brit Nacke ◽  
Borros M. Arneth ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Yi-Chia Lin ◽  
Po-Cheng Liao ◽  
Te-Fu Tsai ◽  
Kuang-Yu Chou ◽  
Hung-En Chen ◽  
...  

Zoledronic acid (ZA), a bisphosphonate used to prevent skeletal fractures in patients with cancers, was demonstrated to induce apoptosis in a number of cancer cells. Our previous study showed that ZA also induces autophagic cell death in metastatic prostate cancer cells. However, the clinical trials using ZA in the treatment of metastatic prostate cancer did not have a longer diseases-free period. Since most of ZA was attracted to the bone after administration, we hypothesized that local prostate cancer cells may evolve prosurvival pathways upon low concentration of ZA treatment. In this study, we investigated the inflammatory effects of ZA on osteolytic PC3 prostate cancer cell, since inflammation was reported to be related to cancer development and survival. Exposure of PC3 cells to various concentrations of ZA resulted in induction of apoptosis and autophagy. The expression of inflammatory biomarkers including interleukin 6 (IL-6), cyclooxygenase-2 (COX-2), and NF-κB was remarkably upregulated in response to ZA treatment in a dose- and time-dependent manner. The production of IL-6 was elevated upon ZA treatment. The antiapoptotic protein Bcl2 was increased with parallel increased level of IL-6. Our data suggest that treatment with low concentrations of ZA enhances the inflammatory profile and may serve as a prosurvival signaling pathway in PC3 cells.


2020 ◽  
Vol 295 (24) ◽  
pp. 8252-8261 ◽  
Author(s):  
C. Alicia Traughber ◽  
Emmanuel Opoku ◽  
Gregory Brubaker ◽  
Jennifer Major ◽  
Hanxu Lu ◽  
...  

High-density lipoprotein (HDL) metabolism is facilitated in part by scavenger receptor class B, type 1 (SR-B1) that mediates HDL uptake into cells. Higher levels of HDL have been associated with protection in other diseases, however, its role in prostate cancer is not definitive. SR-B1 is up-regulated in prostate cancer tissue, suggesting a possible role of this receptor in tumor progression. Here, we report that knockout (KO) of SR-B1 in both human and mouse prostate cancer cell lines through CRISPR/Cas9-mediated genome editing reduces HDL uptake into the prostate cancer cells and reduces their proliferation in response to HDL. In vivo studies using syngeneic SR-B1 WT (SR-B1+/+) and SR-B1 KO (SR-B1−/−) prostate cancer cells in WT and apolipoprotein-AI KO (apoA1-KO) C57BL/6J mice revealed that WT hosts, containing higher levels of total and HDL-cholesterol, grew larger tumors than apoA1-KO hosts with lower levels of total and HDL-cholesterol. Furthermore, SR-B1−/− prostate cancer cells formed smaller tumors in WT hosts than SR-B1+/+ cells in the same host model. Increased tumor volume was overall associated with reduced survival. We conclude that knocking out SR-B1 in prostate cancer tumors reduces HDL-associated increases in prostate cancer cell proliferation and disease progression.


The Prostate ◽  
2010 ◽  
Vol 71 (2) ◽  
pp. 125-133 ◽  
Author(s):  
Eva Wieckowski ◽  
Gurkamal S. Chatta ◽  
Robbie M. Mailliard ◽  
William Gooding ◽  
Karolina Palucka ◽  
...  

The Prostate ◽  
2010 ◽  
Vol 71 (9) ◽  
pp. 964-975 ◽  
Author(s):  
Koji Hoshino ◽  
Hitoshi Ishiguro ◽  
Jun-ichi Teranishi ◽  
Shin-ichiro Yoshida ◽  
Satoshi Umemura ◽  
...  

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