scholarly journals Correlation of Sprouty1 and Jagged1 With Aggressive Prostate Cancer Cells With Different Sensitivities to Androgen Deprivation

2014 ◽  
Vol 115 (9) ◽  
pp. 1505-1515 ◽  
Author(s):  
Naoki Terada ◽  
Takumi Shiraishi ◽  
Yu Zeng ◽  
Koh-Meng Aw-Yong ◽  
Steven M. Mooney ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Androgen Deprivation ◽  
Prostate Cancer Cells ◽  
Aggressive Prostate Cancer

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 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

scholarly journals PlexinB1 Promotes Nuclear Translocation of the Glucocorticoid Receptor

Cells ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 3
Author(s):  
Magali Williamson ◽  
Ritu Garg ◽  
Claire M. Wells
Keyword(s):  
Prostate Cancer ◽  
Glucocorticoid Receptor ◽  
Cancer Cells ◽  
Androgen Deprivation Therapy ◽  
Late Stage ◽  
Nuclear Translocation ◽  
Androgen Deprivation ◽  
Nuclear Localization Sequence ◽  
Prostate Cancer Cells ◽  
Localization Sequence

Androgen receptor (AR) and glucocorticoid receptor (GR) are nuclear receptors whose function depends on their entry into the nucleus where they activate transcription of an overlapping set of genes. Both AR and GR have a role in resistance to androgen deprivation therapy (ADT), the mainstay of treatment for late stage prostate cancer. PlexinB1, a receptor for semaphorins, has been implicated in various cancers including prostate cancer and has a role in resistance to ADT. We show here that activation of PlexinB1 by Sema4D and Sema3C results in translocation of endogenous GR to the nucleus in prostate cancer cells, and that this effect is dependent on PlexinB1 expression. Sema4D/Sema3C promotes the translocation of GR-GFP to the nucleus and mutation of the nuclear localization sequence (NLS1) of GR abrogates this response. These findings implicate the importin α/β system in the Sema4D/Sema3C-mediated nuclear import of GR. Knockdown of PlexinB1 in prostate cancer cells decreases the levels of glucocorticoid-responsive gene products and antagonizes the decrease in cell motility and cell area of prostate cancer cells upon dexamethasone treatment, demonstrating the functional significance of these findings. These results show that PlexinB1 activation has a role in the trafficking and activation of the nuclear receptor GR and thus may have a role in resistance to androgen deprivation therapy in late stage prostate cancer.

scholarly journals PrLZ Protects Prostate Cancer Cells from Apoptosis Induced by Androgen Deprivation via the Activation of Stat3/Bcl-2 Pathway

2011 ◽  
Vol 71 (6) ◽  
pp. 2193-2202 ◽  
Author(s):  
Dong Zhang ◽  
Dalin He ◽  
Yan Xue ◽  
Ruoxiang Wang ◽  
Kaijie Wu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Androgen Deprivation ◽  
Prostate Cancer Cells
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