Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms
- Autores
- Zhi, Gang Li; Mathew, Paul; Yang, Jun; Starbuck, Michael W.; Zurita, Amado J.; Liu, Jie; Sikes, Charles; Multani, Asha S.; Efstathiou, Eleni; Lopez, Adriana; Wang, Jing; Fanning, Tina V.; Prieto, Victor G.; Kundra, Vikas; Vazquez, Elba Susana; Troncoso, Patricia; Raymond, Austin K.; Logothetis, Christopher J.; Lin, Sue-Hwa; Maity, Sankar; Navone, Nora M.
- Año de publicación
- 2008
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- In prostate cancer, androgen blockade strategies are commonly used to treat osteoblastic bone metastases. However, responses to these therapies are typically brief, and the mechanism underlying androgen-independent progression is not clear. Here, we established what we believe to be the first human androgen receptor-negative prostate cancer xenografts whose cells induced an osteoblastic reaction in bone and in the subcutis of immunodeficient mice. Accordingly, these cells grew in castrated as well as intact male mice. We identified FGF9 as being overexpressed in the xenografts relative to other bone-derived prostate cancer cells and discovered that FGF9 induced osteoblast proliferation and new bone formation in a bone organ assay. Mice treated with FGF9-neutralizing antibody developed smaller bone tumors and reduced bone formation. Finally, we found positive FGF9 immunostaining in prostate cancer cells in 24 of 56 primary tumors derived from human organ-confined prostate cancer and in 25 of 25 bone metastasis cases studied. Collectively, these results suggest that FGF9 contributes to prostate cancer-induced new bone formation and may participate in the osteoblastic progression of prostate cancer in bone. Androgen receptor-null cells may contribute to the castration-resistant osteoblastic progression of prostate cancer cells in bone and provide a preclinical model for studying therapies that target these cells.
Fil: Zhi, Gang Li. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Mathew, Paul. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Yang, Jun. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Starbuck, Michael W.. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Zurita, Amado J.. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Liu, Jie. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Sikes, Charles. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Multani, Asha S.. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Efstathiou, Eleni. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Lopez, Adriana. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Wang, Jing. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Fanning, Tina V.. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Prieto, Victor G.. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Kundra, Vikas. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Vazquez, Elba Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Troncoso, Patricia. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Raymond, Austin K.. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Logothetis, Christopher J.. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Lin, Sue-Hwa. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Maity, Sankar. University Of Texas Md Anderson Cancer Center; Estados Unidos
Fil: Navone, Nora M.. University Of Texas Md Anderson Cancer Center; Estados Unidos - Materia
-
PROSTATE CANCER
FGF 9
CASTRATION RESISTANT
OSTEOBLASTIC BONE METASTASIS - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/71291
Ver los metadatos del registro completo
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Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanismsZhi, Gang LiMathew, PaulYang, JunStarbuck, Michael W.Zurita, Amado J.Liu, JieSikes, CharlesMultani, Asha S.Efstathiou, EleniLopez, AdrianaWang, JingFanning, Tina V.Prieto, Victor G.Kundra, VikasVazquez, Elba SusanaTroncoso, PatriciaRaymond, Austin K.Logothetis, Christopher J.Lin, Sue-HwaMaity, SankarNavone, Nora M.PROSTATE CANCERFGF 9CASTRATION RESISTANTOSTEOBLASTIC BONE METASTASIShttps://purl.org/becyt/ford/1.4https://purl.org/becyt/ford/1In prostate cancer, androgen blockade strategies are commonly used to treat osteoblastic bone metastases. However, responses to these therapies are typically brief, and the mechanism underlying androgen-independent progression is not clear. Here, we established what we believe to be the first human androgen receptor-negative prostate cancer xenografts whose cells induced an osteoblastic reaction in bone and in the subcutis of immunodeficient mice. Accordingly, these cells grew in castrated as well as intact male mice. We identified FGF9 as being overexpressed in the xenografts relative to other bone-derived prostate cancer cells and discovered that FGF9 induced osteoblast proliferation and new bone formation in a bone organ assay. Mice treated with FGF9-neutralizing antibody developed smaller bone tumors and reduced bone formation. Finally, we found positive FGF9 immunostaining in prostate cancer cells in 24 of 56 primary tumors derived from human organ-confined prostate cancer and in 25 of 25 bone metastasis cases studied. Collectively, these results suggest that FGF9 contributes to prostate cancer-induced new bone formation and may participate in the osteoblastic progression of prostate cancer in bone. Androgen receptor-null cells may contribute to the castration-resistant osteoblastic progression of prostate cancer cells in bone and provide a preclinical model for studying therapies that target these cells.Fil: Zhi, Gang Li. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Mathew, Paul. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Yang, Jun. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Starbuck, Michael W.. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Zurita, Amado J.. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Liu, Jie. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Sikes, Charles. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Multani, Asha S.. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Efstathiou, Eleni. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Lopez, Adriana. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Wang, Jing. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Fanning, Tina V.. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Prieto, Victor G.. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Kundra, Vikas. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Vazquez, Elba Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Troncoso, Patricia. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Raymond, Austin K.. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Logothetis, Christopher J.. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Lin, Sue-Hwa. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Maity, Sankar. University Of Texas Md Anderson Cancer Center; Estados UnidosFil: Navone, Nora M.. University Of Texas Md Anderson Cancer Center; Estados UnidosAmerican Society for Clinical Investigation2008-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/71291Zhi, Gang Li; Mathew, Paul; Yang, Jun; Starbuck, Michael W.; Zurita, Amado J.; et al.; Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms; American Society for Clinical Investigation; Journal of Clinical Investigation; 118; 8; 8-2008; 2697-27100021-9738CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1172/JCI33093info:eu-repo/semantics/altIdentifier/url/https://www.jci.org/articles/view/33093info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:08:00Zoai:ri.conicet.gov.ar:11336/71291instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:08:01.15CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms |
| title |
Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms |
| spellingShingle |
Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms Zhi, Gang Li PROSTATE CANCER FGF 9 CASTRATION RESISTANT OSTEOBLASTIC BONE METASTASIS |
| title_short |
Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms |
| title_full |
Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms |
| title_fullStr |
Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms |
| title_full_unstemmed |
Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms |
| title_sort |
Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms |
| dc.creator.none.fl_str_mv |
Zhi, Gang Li Mathew, Paul Yang, Jun Starbuck, Michael W. Zurita, Amado J. Liu, Jie Sikes, Charles Multani, Asha S. Efstathiou, Eleni Lopez, Adriana Wang, Jing Fanning, Tina V. Prieto, Victor G. Kundra, Vikas Vazquez, Elba Susana Troncoso, Patricia Raymond, Austin K. Logothetis, Christopher J. Lin, Sue-Hwa Maity, Sankar Navone, Nora M. |
| author |
Zhi, Gang Li |
| author_facet |
Zhi, Gang Li Mathew, Paul Yang, Jun Starbuck, Michael W. Zurita, Amado J. Liu, Jie Sikes, Charles Multani, Asha S. Efstathiou, Eleni Lopez, Adriana Wang, Jing Fanning, Tina V. Prieto, Victor G. Kundra, Vikas Vazquez, Elba Susana Troncoso, Patricia Raymond, Austin K. Logothetis, Christopher J. Lin, Sue-Hwa Maity, Sankar Navone, Nora M. |
| author_role |
author |
| author2 |
Mathew, Paul Yang, Jun Starbuck, Michael W. Zurita, Amado J. Liu, Jie Sikes, Charles Multani, Asha S. Efstathiou, Eleni Lopez, Adriana Wang, Jing Fanning, Tina V. Prieto, Victor G. Kundra, Vikas Vazquez, Elba Susana Troncoso, Patricia Raymond, Austin K. Logothetis, Christopher J. Lin, Sue-Hwa Maity, Sankar Navone, Nora M. |
| author2_role |
author author author author author author author author author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
PROSTATE CANCER FGF 9 CASTRATION RESISTANT OSTEOBLASTIC BONE METASTASIS |
| topic |
PROSTATE CANCER FGF 9 CASTRATION RESISTANT OSTEOBLASTIC BONE METASTASIS |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.4 https://purl.org/becyt/ford/1 |
| dc.description.none.fl_txt_mv |
In prostate cancer, androgen blockade strategies are commonly used to treat osteoblastic bone metastases. However, responses to these therapies are typically brief, and the mechanism underlying androgen-independent progression is not clear. Here, we established what we believe to be the first human androgen receptor-negative prostate cancer xenografts whose cells induced an osteoblastic reaction in bone and in the subcutis of immunodeficient mice. Accordingly, these cells grew in castrated as well as intact male mice. We identified FGF9 as being overexpressed in the xenografts relative to other bone-derived prostate cancer cells and discovered that FGF9 induced osteoblast proliferation and new bone formation in a bone organ assay. Mice treated with FGF9-neutralizing antibody developed smaller bone tumors and reduced bone formation. Finally, we found positive FGF9 immunostaining in prostate cancer cells in 24 of 56 primary tumors derived from human organ-confined prostate cancer and in 25 of 25 bone metastasis cases studied. Collectively, these results suggest that FGF9 contributes to prostate cancer-induced new bone formation and may participate in the osteoblastic progression of prostate cancer in bone. Androgen receptor-null cells may contribute to the castration-resistant osteoblastic progression of prostate cancer cells in bone and provide a preclinical model for studying therapies that target these cells. Fil: Zhi, Gang Li. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Mathew, Paul. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Yang, Jun. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Starbuck, Michael W.. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Zurita, Amado J.. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Liu, Jie. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Sikes, Charles. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Multani, Asha S.. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Efstathiou, Eleni. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Lopez, Adriana. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Wang, Jing. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Fanning, Tina V.. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Prieto, Victor G.. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Kundra, Vikas. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Vazquez, Elba Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina Fil: Troncoso, Patricia. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Raymond, Austin K.. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Logothetis, Christopher J.. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Lin, Sue-Hwa. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Maity, Sankar. University Of Texas Md Anderson Cancer Center; Estados Unidos Fil: Navone, Nora M.. University Of Texas Md Anderson Cancer Center; Estados Unidos |
| description |
In prostate cancer, androgen blockade strategies are commonly used to treat osteoblastic bone metastases. However, responses to these therapies are typically brief, and the mechanism underlying androgen-independent progression is not clear. Here, we established what we believe to be the first human androgen receptor-negative prostate cancer xenografts whose cells induced an osteoblastic reaction in bone and in the subcutis of immunodeficient mice. Accordingly, these cells grew in castrated as well as intact male mice. We identified FGF9 as being overexpressed in the xenografts relative to other bone-derived prostate cancer cells and discovered that FGF9 induced osteoblast proliferation and new bone formation in a bone organ assay. Mice treated with FGF9-neutralizing antibody developed smaller bone tumors and reduced bone formation. Finally, we found positive FGF9 immunostaining in prostate cancer cells in 24 of 56 primary tumors derived from human organ-confined prostate cancer and in 25 of 25 bone metastasis cases studied. Collectively, these results suggest that FGF9 contributes to prostate cancer-induced new bone formation and may participate in the osteoblastic progression of prostate cancer in bone. Androgen receptor-null cells may contribute to the castration-resistant osteoblastic progression of prostate cancer cells in bone and provide a preclinical model for studying therapies that target these cells. |
| publishDate |
2008 |
| dc.date.none.fl_str_mv |
2008-08 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
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publishedVersion |
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http://hdl.handle.net/11336/71291 Zhi, Gang Li; Mathew, Paul; Yang, Jun; Starbuck, Michael W.; Zurita, Amado J.; et al.; Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms; American Society for Clinical Investigation; Journal of Clinical Investigation; 118; 8; 8-2008; 2697-2710 0021-9738 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/71291 |
| identifier_str_mv |
Zhi, Gang Li; Mathew, Paul; Yang, Jun; Starbuck, Michael W.; Zurita, Amado J.; et al.; Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms; American Society for Clinical Investigation; Journal of Clinical Investigation; 118; 8; 8-2008; 2697-2710 0021-9738 CONICET Digital CONICET |
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eng |
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eng |
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info:eu-repo/semantics/altIdentifier/doi/10.1172/JCI33093 info:eu-repo/semantics/altIdentifier/url/https://www.jci.org/articles/view/33093 |
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American Society for Clinical Investigation |
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American Society for Clinical Investigation |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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