The Expression of Sprouty1, an Inhibitor of Fibroblast Growth Factor Signal Transduction, Is Decreased in Human Prostate Cancer
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- Bernard Kwabi-Addo
- 1Department of Pathology, Baylor College of Medicine, and
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- Jianghua Wang
- 1Department of Pathology, Baylor College of Medicine, and
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- Halime Erdem
- 1Department of Pathology, Baylor College of Medicine, and
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- Ajula Vaid
- 1Department of Pathology, Baylor College of Medicine, and
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- Patricia Castro
- 1Department of Pathology, Baylor College of Medicine, and
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- Gustavo Ayala
- 1Department of Pathology, Baylor College of Medicine, and
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- Michael Ittmann
- 1Department of Pathology, Baylor College of Medicine, and
抄録
<jats:title>Abstract</jats:title> <jats:p>A considerable body of evidence indicates that alterations of fibroblast growth factors (FGFs) and their receptors contribute to prostate cancer progression. Recently, a new family of regulators of FGF activity has been identified. The Sprouty gene family negatively regulates FGF signaling in a variety of systems and could potentially limit the biological activity of FGFs in prostate cancer. Immunohistochemical analysis of normal and neoplastic prostate tissues using tissue microarrays revealed that Sprouty1 protein is down-regulated in approximately 40% of prostate cancers when compared with matched normal prostate. By quantitative real-time PCR analysis, we found that Sprouty1 mRNA levels were significantly decreased in prostate cancers in vivo in comparison with normal prostate. In prostate cancer cell lines, there is loss of the normal up-regulation of Sprouty1 mRNA and protein in response to FGFs. The decrease in Sprouty1 expression in the human prostate cancer, despite elevated levels of FGF ligands and FGF receptors, implies a loss of an important growth regulatory mechanism in prostate cancers that may potentiate the effects of increased FGF and FGF receptor expression in prostate cancer.</jats:p>
収録刊行物
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- Cancer Research
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Cancer Research 64 (14), 4728-4735, 2004-07-15
American Association for Cancer Research (AACR)
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詳細情報 詳細情報について
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- CRID
- 1363107368465869056
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- NII論文ID
- 30018590391
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- ISSN
- 15387445
- 00085472
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