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Bone morphogenetic protein signaling in prostate cancer cell lines
Author(s) -
Brubaker K.D.,
Corey E.,
Brown L.G.,
Vessella R.L.
Publication year - 2003
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.10679
Subject(s) - lncap , bone morphogenetic protein , prostate cancer , cancer research , smad , bone morphogenetic protein 4 , osteoprotegerin , bone morphogenetic protein 7 , bone morphogenetic protein 2 , prostate , medicine , cancer , endocrinology , biology , transforming growth factor , receptor , biochemistry , activator (genetics) , in vitro , gene
Prostate cancer is the most commonly diagnosed malignancy in men and is often associated with bone metastases. Prostate cancer bone lesions can be lytic or schlerotic, with the latter predominating. Bone morphogenetic proteins (BMPs) are a family of growth factors, which may play a role in the formation of prostate cancer osteoblastic bone metastases. This study evaluated the effects of BMPs on prostate cancer cell lines. We observed growth inhibitory effects of BMP‐2 and ‐4 on LNCaP, while PC‐3 was unaffected. Flow cytometric analysis determined that LNCaP cell growth was arrested in G 1 after bone morphogenetic protein‐2 treatment. Treatment of LNCaP and PC‐3 with BMP‐2 and ‐4 activated downstream signaling pathways involving SMAD‐1, up‐regulation of p21 CIP1/WAF1 and changes in retinoblastoma (Rb) phosphorylation. Interestingly, bone morphogenetic protein‐2 treatment stimulated a 2.7‐fold increase in osteoprotegerin (OPG), a molecule, which inhibits osteoclastogenesis, production in PC‐3. © 2003 Wiley‐Liss, Inc.