Dong Han, Maryam Labaf, Yawei Zhao, Jude Owiredu, Songqi Zhang, Krishna Patel, Kavita Venkataramani, Jocelyn S Steinfeld, Wanting Han, Muqing Li, Mingyu Liu, Zifeng Wang, Anna Besschetnova, Susan Patalano, Michaela J Mulhearn, Jill A Macoska, Xin Yuan, Steven P Balk, Peter S Nelson, Stephen R Plymate, Shuai Gao, Kellee R Siegfried, Ruihua Liu, Mary M Stangis, Gabrielle Foxa, Piotr J Czernik, Bart O Williams, Kourosh Zarringhalam, Xiaohong Li, Changmeng Cai
One critical mechanism through which prostate cancer (PCa) adapts to treatments targeting androgen receptor (AR) signaling is the emergence of ligand-binding domain-truncated and constitutively active AR splice variants, particularly AR-V7. While AR-V7 has been intensively studied, its ability to activate distinct biological functions compared to the full-length AR (AR-FL), and its role in regulating the metastatic progression of castration-resistant PCa (CRPC), remains unclear. Our study found that, under castrated conditions, AR-V7 strongly induced osteoblastic bone lesions, a response not observed with AR-FL overexpression...
April 30, 2024: Journal of Clinical Investigation