scholarly journals Expression of Human Prostatic Acid Phosphatase Correlates with Androgen-stimulated Cell Proliferation in Prostate Cancer Cell Lines

1998 ◽  
Vol 273 (10) ◽  
pp. 5939-5947 ◽  
Author(s):  
Ming-Fong Lin ◽  
Tzu-Ching Meng ◽  
Prathibha S. Rao ◽  
Chawnshang Chang ◽  
Axel H. Schönthal ◽  
...  
2014 ◽  
Vol 32 (4_suppl) ◽  
pp. 281-281
Author(s):  
Benjamin C. Powers ◽  
Bhaskar Das ◽  
Boumediene Bouzahzah ◽  
Peter J. Van Veldhuizen ◽  
Emma Borrego-Diaz Reyes

281 Background: Prostate cancer is the second most common cancer worldwide in males. The initial treatment in advanced cases is medical or surgical castration. The outlook declines when prostate cancer advances independently, despite the aforementioned castration. Within the last ten years, a handful of new agents have proven effective in this castration-resistant phase, but finding more effective, novel ways of treating advanced prostate cancer is warranted. MAGMAS (mitochondria-associated, granulocyte-macrophage colony stimulating factor (GM-CSF) signaling molecule) is a protein ubiquitously expressed in eukaryotic cells that plays a key role in embryonal development in a variety of species. Overexpression of MAGMAS has anti-apoptotic effects, as GM-CSF is a growth factor essential for survival, proliferation and differentiation of cells. MAGMAS and GM-CSF receptor levels have been shown to be overexpressed in prostate cancer, but do not correlate with pathological grade or clinical stage. The purpose of our study was to evaluate the efficacy of a MAGMAS inhibitor, synthesized by Dr Bhaskar Das, in androgen-dependent and androgen-independent prostate cancer cell lines, as well as in a normal prostate cell line as another control. Methods: The different cell lines were treated with MAGMAS inhibitor at various concentrations in vitro. For analysis, we used MTT Cell Proliferation assay at 24 and 48 hours, per manufacturer’s protocol. We tested MAGMAS inhibitor effect on apoptosis/necrosis, cell migration and microtubule destabilization as well. Results: After prostate cancer cell lines were treated with MAGMAS inhibitor in vitro, cell proliferation and migration decreased, apoptosis and necrosis were induced, and microtubules were destabilized, all showing more impressive results in the androgen-independent cells. MAGMAS inhibition did not affect cell proliferation in the normal prostate cells. Conclusions: In vitro studies show MAGMAS inhibition proves efficacious in both androgen-dependent and androgen-independent prostate cancer cell lines. This will be evaluated further in a xenograft mouse model.


Tumor Biology ◽  
2010 ◽  
Vol 31 (4) ◽  
pp. 297-307 ◽  
Author(s):  
Modjtaba Emadi Baygi ◽  
Zahra-Soheila Soheili ◽  
Frank Essmann ◽  
Abdolkhaleg Deezagi ◽  
Rainer Engers ◽  
...  

Author(s):  
Abdul-Nazif Mahmud ◽  
Feilun Cui ◽  
Xue Bo ◽  
Jianpeng Hu ◽  
Tingjun Liu ◽  
...  

<p><strong>Background:</strong> SIRT4 is among the few characterized individual sirtuin groups of nicotinamide adenine dinucleotide-dependent enzymes base in the mitochondria that facilitate several significant processes at the cellular level including stress response, metabolism and longevity. SIRT4 can suppress and inhibits the growth, proliferation and transformation of tumor cells such as colorectal and gastric tumors by suppressing glutamine anaplerosis, but there is no research that reveal the role and function SIRT4 plays in the development of prostate tumor.</p> <p><strong>Methods:</strong> Overexpression of SIRT4 in prostate cancer cell lines LNCaP was determined using RT-qPCR and Western blotting analyses. CCK-8 and transwell analysis were utilized to establish SIRT4 overexpression effects on cell proliferation and cell invasion respectively.</p> <p><strong>Results:</strong> This study first established SIRT4 overexpression in prostate cancer cell lines LNCaP, functional experiment such as CCK-8 assay reveals that, overexpression of SIRT4 suppressed cell proliferation. In addition, transwell assay reveals that, SIRT4 overexpression inhibits cell invasion.</p> <p><strong>Conclusions:</strong> This research findings reveals that, SIRT4 function to suppress prostate cancer cells by impeding the proliferation and invasion of LNCaP cells. SIRT4 may serve as a new treatment target for prostate tumor.</p>


Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831769453 ◽  
Author(s):  
Yifan Liu ◽  
Shan Zeng ◽  
Xianhan Jiang ◽  
Dehui Lai ◽  
Zhengming Su

SOX4 (sex-determining region Y-related high-mobility group box 4) is associated with tumor progression and poor clinical outcome in several cancers. This study aims to evaluate whether SOX4 affects the biological behaviors of prostate cancer and further elucidate whether this effect works through the epithelial–mesenchymal transition pathway. We investigated the expression of SOX4 in a series of prostate cancer tissues and adjacent noncancerous tissues, as well as in a panel of prostate cancer cell lines. Cell proliferation, migration, and invasion were evaluated in SOX4 knockdown prostate cancer cell lines by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assay. Our results showed that the expression of SOX4 was remarkably upregulated both in prostate cancer tissues and in cell lines. Knockdown of SOX4 repressed the ability of cell proliferation and migration of DU145 cells. Moreover, inhibition of SOX4 could reverse the epithelial–mesenchymal transition processes through upregulation of E-cadherin and downregulation of vimentin. This study provided evidence that SOX4 could serve as a potential therapeutic target in prostate cancer.


2006 ◽  
Vol 175 (4S) ◽  
pp. 258-258
Author(s):  
Ruth Schwaninger ◽  
Cyrill A. Rentsch ◽  
Antoinette Wetterwald ◽  
Irena Klima ◽  
Gabri Van der Pluijm ◽  
...  

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