Human ASH-1 Promotes Neuroendocrine Differentiation in Androgen Deprivation Conditions and Interferes With Androgen Responsiveness in Prostate Cancer Cells

The Prostate ◽  
2013 ◽  
Vol 73 (11) ◽  
pp. 1241-1249 ◽  
Author(s):  
Ida Rapa ◽  
Marco Volante ◽  
Cristina Migliore ◽  
Antonella Farsetti ◽  
Alfredo Berruti ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Neuroendocrine Differentiation ◽  
Androgen Deprivation ◽  
Prostate Cancer Cells

scholarly journals SHH-N non-canonically sustains androgen receptor activity in androgen-independent prostate cancer cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Diana Trnski ◽  
Maja Sabol ◽  
Sanja Tomić ◽  
Ivan Štefanac ◽  
Milanka Mrčela ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Therapy Resistance ◽  
Androgen Deprivation ◽  
Prostate Cancer Cells ◽  
Androgen Independence ◽  
Androgen Receptor Activity ◽  
Signaling Activation ◽  
Androgen Independent

AbstractProstate cancer is the second most frequent cancer diagnosed in men worldwide. Localized disease can be successfully treated, but advanced cases are more problematic. After initial effectiveness of androgen deprivation therapy, resistance quickly occurs. Therefore, we aimed to investigate the role of Hedgehog-GLI (HH-GLI) signaling in sustaining androgen-independent growth of prostate cancer cells. We found various modes of HH-GLI signaling activation in prostate cancer cells depending on androgen availability. When androgen was not deprived, we found evidence of non-canonical SMO signaling through the SRC kinase. After short-term androgen deprivation canonical HH-GLI signaling was activated, but we found little evidence of canonical HH-GLI signaling activity in androgen-independent prostate cancer cells. We show that in androgen-independent cells the pathway ligand, SHH-N, non-canonically binds to the androgen receptor through its cholesterol modification. Inhibition of this interaction leads to androgen receptor signaling downregulation. This implies that SHH-N activates the androgen receptor and sustains androgen-independence. Targeting this interaction might prove to be a valuable strategy for advanced prostate cancer treatment. Also, other non-canonical aspects of this signaling pathway should be investigated in more detail and considered when developing potential therapies.

scholarly journals Overexpression of an α1H(Cav3.2) T-type Calcium Channel during Neuroendocrine Differentiation of Human Prostate Cancer Cells

2002 ◽  
Vol 277 (13) ◽  
pp. 10824-10833 ◽  
Author(s):  
Pascal Mariot ◽  
Karine Vanoverberghe ◽  
Nathalie Lalevée ◽  
Michel F. Rossier ◽  
Natalia Prevarskaya
Keyword(s):  
Prostate Cancer ◽  
Calcium Channel ◽  
Cancer Cells ◽  
Neuroendocrine Differentiation ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

scholarly journals Persistence of senescent prostate cancer cells following prolonged neoadjuvant androgen deprivation therapy

PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0172048 ◽  
Author(s):  
Michael L. Blute ◽  
Nathan Damaschke ◽  
Jennifer Wagner ◽  
Bing Yang ◽  
Martin Gleave ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Androgen Deprivation Therapy ◽  
Androgen Deprivation ◽  
Prostate Cancer Cells

scholarly journals Androgen Deprivation Followed by Acute Androgen Stimulation Selectively Sensitizes AR-Positive Prostate Cancer Cells to Ionizing Radiation

2016 ◽  
Vol 22 (13) ◽  
pp. 3310-3319 ◽  
Author(s):  
Mohammad Hedayati ◽  
Michael C. Haffner ◽  
Jonathan B. Coulter ◽  
Raju R. Raval ◽  
Yonggang Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Ionizing Radiation ◽  
Cancer Cells ◽  
Androgen Deprivation ◽  
Prostate Cancer Cells
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