Interference with the androgen receptor protein stability in therapy‐resistant prostate cancer

2018 ◽  
Vol 144 (8) ◽  
pp. 1775-1779 ◽  
Author(s):  
Gopinath Lakshmana ◽  
Aria Baniahmad
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Protein Stability ◽  
Receptor Protein ◽  
Androgen Receptor Protein

Dynamic rewiring of the androgen receptor protein interaction network correlates with prostate cancer clinical outcomes

2011 ◽  
Vol 3 (10) ◽  
pp. 1020 ◽  
Author(s):  
Miltiadis Paliouras ◽  
Naif Zaman ◽  
Rose Lumbroso ◽  
Laurie Kapogeorgakis ◽  
Lenore K. Beitel ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Clinical Outcomes ◽  
Protein Interaction ◽  
Protein Interaction Network ◽  
Interaction Network ◽  
Receptor Protein ◽  
Androgen Receptor Protein

scholarly journals A Systematic Comparison of Antiandrogens Identifies Androgen Receptor Protein Stability as an Indicator for Treatment Response

Life ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 874
Author(s):  
Tiziana Siciliano ◽  
Ingo H. Simons ◽  
Alicia-Marie K. Beier ◽  
Celina Ebersbach ◽  
Cem Aksoy ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Cell Viability ◽  
Protein Stability ◽  
Primary Treatment ◽  
Receptor Protein ◽  
Androgen Receptor Protein ◽  
Antiandrogen Therapy ◽  
Level Reduction ◽  
Androgen Independent

Antiandrogen therapy is a primary treatment for patients with metastasized prostate cancer. Whilst the biologic mechanisms of antiandrogens have been extensively studied, the operating protocols used for the characterization of these drugs were not identical, limiting their comparison. Here, the antiandrogens Bicalutamide, Enzalutamide, Apalutamide, and Darolutamide were systematically compared using identical experimental setups. Androgen-dependent LNCaP and LAPC4 cells as well as androgen-independent C4-2 cells were treated with distinct concentrations of antiandrogens. Androgen receptor (AR)-mediated gene transactivation was determined using qPCR. Cell viability was measured by WST1 assay. Protein stability and AR localization were determined using western blot. Response to the tested antiandrogens across cellular backgrounds differed primarily in AR-mediated gene transactivation and cell viability. Antiandrogen treatment in LNCaP and LAPC4 cells resulted in AR protein level reduction, whereas in C4-2 cells marginal decreased AR protein was observed after treatment. In addition, AR downregulation was already detectable after 4 h, whereas reduced AR-mediated gene transactivation was not observed before 6 h. None of the tested antiandrogens displayed an advantage on the tested parameters within one cell line as opposed to the cellular background, which seems to be the primary influence on antiandrogen efficacy. Moreover, the results revealed a prominent role in AR protein stability. It is one of the first events triggered by antiandrogens and correlated with antiandrogen efficiency. Therefore, AR stability may surrogate antiandrogen response and may be a possible target to reverse antiandrogen resistance.

114. Androgen receptor protein expression influences freeze sensitivity of prostate cancer cells

Cryobiology ◽  
2007 ◽  
Vol 55 (3) ◽  
pp. 362
Author(s):  
John G. Baust ◽  
Daniel P. Klossner ◽  
Dominic M. Clarke ◽  
Robert G. Van Buskirk ◽  
Andrew A. Gage ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Protein Expression ◽  
Cancer Cells ◽  
Receptor Protein ◽  
Prostate Cancer Cells ◽  
Androgen Receptor Protein
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