High mobility group protein AT-hook 1 (HMGA1) is associated with the development of androgen independence in prostate cancer cells

The Prostate ◽  
2011 ◽  
Vol 72 (10) ◽  
pp. 1124-1132 ◽  
Author(s):  
Ichiro Takeuchi ◽  
Natsuki Takaha ◽  
Terukazu Nakamura ◽  
Fumiya Hongo ◽  
Kazuya Mikami ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
High Mobility ◽  
High Mobility Group ◽  
Prostate Cancer Cells ◽  
High Mobility Group Protein ◽  
Androgen Independence ◽  
Group Protein

Nuclear matrix localization of high mobility group protein I(Y) in a transgenic mouse model for prostate cancer

2002 ◽  
Vol 88 (3) ◽  
pp. 599-608 ◽  
Author(s):  
Eddy S. Leman ◽  
Michael C. Madigan ◽  
Gisela Brünagel ◽  
Natsuki Takaha ◽  
Donald S. Coffey ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Nuclear Matrix ◽  
High Mobility ◽  
Transgenic Mouse Model ◽  
High Mobility Group ◽  
High Mobility Group Protein ◽  
Group Protein

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.

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