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Follistatin drives AR-independent prostate cancer through BMP signaling inactivation and microenvironmental remodeling.

Xiaoxian Shi, Zuyan Fan, Min Qu, Chunjie Lin, Zhiheng Ji, Caiwei Tan, Biqi Dai, Rushan Chen, Yixuan Du, Yizhong Bao, Zhifan Ding, Liqun Xia, Furong Liu, Hongliang Gao, Tianyu Cao, Wei Xie, Dong Fang, Weijie Zhang, Deli Huang, Jun Chen, Xu Gao, Xinhua Feng, Gonghui Li, Jing Li, Wenjing Su

Proceedings of the National Academy of Sciences of the United States of AmericaSep 29, 2026PMID 42784510doi:10.1073/pnas.2603564123 Journal ArticlepubmedProvenance
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PubMed
Retrieved
Sep 29, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Run
ING-PUBMED-20260929-000001
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Resistance to androgen receptor (AR)-targeted therapies remains a major clinical challenge in advanced prostate cancer. Here we identify follistatin (FST), TGFβ superfamily antagonist, as a key driver of AR-independence and treatment resistance. During anti-AR therapy, cancer cells progressively…

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