Prostate cancer bone metastases acquire resistance to androgen deprivation via WNT5A-mediated BMP-6 induction View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-02-11

AUTHORS

G T Lee, D I Kang, Y-S Ha, Y S Jung, J Chung, K Min, T H Kim, K H Moon, J M Chung, D H Lee, W-J Kim, I Y Kim

ABSTRACT

BACKGROUND: Androgen ablation is the first-line therapy for patients with metastatic prostate cancer (CaP). However, castration resistance will eventually emerge. In the present study, we have investigated the role of bone morphogenetic protein-6 (BMP-6) in the development of castration-resistant prostate cancer (CRPC) in the context of bone metastases. METHODS: We initially investigated the clinical course of 158 men with advanced CaP who were treated with primary androgen deprivation therapy. To elucidate the underlying mechanism of CRPC in the context of bone metastases, we examined the impact of bone stromal cells on CaP in the absence of androgens using a co-culture model. RESULTS: In the 158 patients, we found that the median time to prostate-specific antigen progression was significantly shorter when bone metastases were present (14 months (95% CI, 10.2-17.8 months) vs 57 months (95% CI, 19.4-94.6 months)). These results suggest that bone-tumour interactions may accelerate castration resistance. Consistent with this hypothesis, in vitro co-cultures demonstrated that CaP cells proliferated under an androgen-depleted condition when incubated with bone stromal cells. Mechanistically, gene expression analysis using quantitative polymerase chain reaction arrays showed a dramatic induction of BMP-6 by CaP cell lines in the presence of bone stromal cells. Further studies revealed that WNT5A derived from bone stromal cells induced the expression of BMP-6 by CaP cells; BMP-6 in turn stimulated cellular proliferation of CaP cells in an androgen-deprived media via a physical interaction between Smad5 and β-catenin. Intracellularly, WNT5A increased BMP-6 expression via protein kinase C/NF-κB pathway in CaP cell lines. CONCLUSIONS: These observations suggest that bone-CaP interaction leads to castration resistance via WNT5A/BMP-6 loop. More... »

PAGES

1634-1644

Journal

TITLE

British Journal of Cancer

ISSUE

6

VOLUME

110

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/bjc.2014.23

DOI

http://dx.doi.org/10.1038/bjc.2014.23

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1033508699

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24518599


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37 schema:description BACKGROUND: Androgen ablation is the first-line therapy for patients with metastatic prostate cancer (CaP). However, castration resistance will eventually emerge. In the present study, we have investigated the role of bone morphogenetic protein-6 (BMP-6) in the development of castration-resistant prostate cancer (CRPC) in the context of bone metastases. METHODS: We initially investigated the clinical course of 158 men with advanced CaP who were treated with primary androgen deprivation therapy. To elucidate the underlying mechanism of CRPC in the context of bone metastases, we examined the impact of bone stromal cells on CaP in the absence of androgens using a co-culture model. RESULTS: In the 158 patients, we found that the median time to prostate-specific antigen progression was significantly shorter when bone metastases were present (14 months (95% CI, 10.2-17.8 months) vs 57 months (95% CI, 19.4-94.6 months)). These results suggest that bone-tumour interactions may accelerate castration resistance. Consistent with this hypothesis, in vitro co-cultures demonstrated that CaP cells proliferated under an androgen-depleted condition when incubated with bone stromal cells. Mechanistically, gene expression analysis using quantitative polymerase chain reaction arrays showed a dramatic induction of BMP-6 by CaP cell lines in the presence of bone stromal cells. Further studies revealed that WNT5A derived from bone stromal cells induced the expression of BMP-6 by CaP cells; BMP-6 in turn stimulated cellular proliferation of CaP cells in an androgen-deprived media via a physical interaction between Smad5 and β-catenin. Intracellularly, WNT5A increased BMP-6 expression via protein kinase C/NF-κB pathway in CaP cell lines. CONCLUSIONS: These observations suggest that bone-CaP interaction leads to castration resistance via WNT5A/BMP-6 loop.
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45 BMP-6 induction
46 BMP-6 loop
47 C/NF-κB pathway
48 CaP cell lines
49 Further studies
50 NF-κB pathway
51 Smad5
52 WNT5A/BMP-6 loop
53 Wnt5a
54 ablation
55 absence
56 absence of androgen
57 advanced CaP
58 analysis
59 androgen ablation
60 androgen deprivation therapy
61 androgen-depleted conditions
62 androgen-deprived medium
63 androgens
64 antigen progression
65 array
66 bone metastases
67 bone morphogenetic protein 6
68 bone stromal cells
69 bone-CaP interaction
70 bone-tumour interactions
71 cancer
72 cancer bone metastasis
73 cap
74 cap cells
75 castration resistance
76 castration-resistant prostate cancer
77 catenin
78 cell lines
79 cells
80 cellular proliferation
81 chain reaction arrays
82 clinical course
83 co-culture model
84 conditions
85 context
86 course
87 deprivation
88 deprivation therapy
89 development
90 dramatic induction
91 expression
92 expression analysis
93 first-line therapy
94 gene expression analysis
95 hypothesis
96 impact
97 induction
98 interaction
99 kinase C/NF-κB pathway
100 lines
101 loop
102 mechanism
103 median time
104 medium
105 men
106 metastasis
107 metastatic prostate cancer
108 model
109 morphogenetic protein-6
110 observations
111 pathway
112 patients
113 physical interaction
114 polymerase chain reaction array
115 presence
116 present study
117 primary androgen deprivation therapy
118 progression
119 proliferation
120 prostate cancer
121 prostate cancer bone metastasis
122 prostate-specific antigen progression
123 protein 6
124 protein kinase C/NF-κB pathway
125 quantitative polymerase chain reaction array
126 reaction arrays
127 resistance
128 results
129 role
130 stromal cells
131 study
132 therapy
133 time
134 turn
135 underlying mechanism
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