PURPOSE: Glucocorticoids such as prednisone, hydrocortisone, and dexamethasone are known to provide some clinical benefit for patients with hormone-refractory prostate cancer. However, the underlying mechanisms by which glucocorticoids affect hormone-refractory prostate cancer progression are not well established as yet. Our previous study has shown that glucocorticoids inhibit tumor angiogenesis possibly by down-regulation of vascular endothelial growth factor (VEGF) and interleukin 8. Here, we hypothesized that the therapeutic effect of dexamethasone on hormone-refractory prostate cancer can be partly attributed to a direct inhibition of lymphangiogenesis through the glucocorticoid receptor by down-regulating a major lymphangiogenic factor, VEGF-C. EXPERIMENTAL DESIGN: The effects of dexamethasone on the expression of VEGF-C and its receptor, VEGF receptor-3 (VEGFR-3), were examined using an androgen-independent human prostate cancer cell line, DU145, which expresses glucocorticoid r
%0 Journal Article
%1 Yano.2006
%A Yano, A.
%A Fujii, Y.
%A Iwai, A.
%A Kawakami, S.
%A Kageyama, Y.
%A Kihara, K.
%D 2006
%J Clin.Cancer Res.
%K & Animals C Cell Chain Dexamethasone Endothelial Expression Factor Gene Glucocorticoids Growth Heterologous Human Humans Japan Line Lymphangiogenesis Lymphatic Male Metastasis Mice Neoplasms Neoplastic Polymerase Prostate Prostatic Reaction Receptor-3 Regulation Reverse Transcriptase Transplantation Tumor Vascular cells control drug effects genetics pathology pharmacology prevention protein
%N 20 Pt 1
%P 6012-6017
%T Glucocorticoids suppress tumor lymphangiogenesis of prostate cancer cells
%U PM:17062674
%V 12
%X PURPOSE: Glucocorticoids such as prednisone, hydrocortisone, and dexamethasone are known to provide some clinical benefit for patients with hormone-refractory prostate cancer. However, the underlying mechanisms by which glucocorticoids affect hormone-refractory prostate cancer progression are not well established as yet. Our previous study has shown that glucocorticoids inhibit tumor angiogenesis possibly by down-regulation of vascular endothelial growth factor (VEGF) and interleukin 8. Here, we hypothesized that the therapeutic effect of dexamethasone on hormone-refractory prostate cancer can be partly attributed to a direct inhibition of lymphangiogenesis through the glucocorticoid receptor by down-regulating a major lymphangiogenic factor, VEGF-C. EXPERIMENTAL DESIGN: The effects of dexamethasone on the expression of VEGF-C and its receptor, VEGF receptor-3 (VEGFR-3), were examined using an androgen-independent human prostate cancer cell line, DU145, which expresses glucocorticoid r
@article{Yano.2006,
abstract = {PURPOSE: Glucocorticoids such as prednisone, hydrocortisone, and dexamethasone are known to provide some clinical benefit for patients with hormone-refractory prostate cancer. However, the underlying mechanisms by which glucocorticoids affect hormone-refractory prostate cancer progression are not well established as yet. Our previous study has shown that glucocorticoids inhibit tumor angiogenesis possibly by down-regulation of vascular endothelial growth factor (VEGF) and interleukin 8. Here, we hypothesized that the therapeutic effect of dexamethasone on hormone-refractory prostate cancer can be partly attributed to a direct inhibition of lymphangiogenesis through the glucocorticoid receptor by down-regulating a major lymphangiogenic factor, VEGF-C. EXPERIMENTAL DESIGN: The effects of dexamethasone on the expression of VEGF-C and its receptor, VEGF receptor-3 (VEGFR-3), were examined using an androgen-independent human prostate cancer cell line, DU145, which expresses glucocorticoid r},
added-at = {2010-02-05T11:28:39.000+0100},
author = {Yano, A. and Fujii, Y. and Iwai, A. and Kawakami, S. and Kageyama, Y. and Kihara, K.},
biburl = {https://www.bibsonomy.org/bibtex/2df8b4bb1902ba2e95f20a9161cb38d39/kanefendt},
interhash = {864acc113707489851930c1caac450e2},
intrahash = {df8b4bb1902ba2e95f20a9161cb38d39},
journal = {Clin.Cancer Res.},
keywords = {& Animals C Cell Chain Dexamethasone Endothelial Expression Factor Gene Glucocorticoids Growth Heterologous Human Humans Japan Line Lymphangiogenesis Lymphatic Male Metastasis Mice Neoplasms Neoplastic Polymerase Prostate Prostatic Reaction Receptor-3 Regulation Reverse Transcriptase Transplantation Tumor Vascular cells control drug effects genetics pathology pharmacology prevention protein},
number = {20 Pt 1},
pages = {6012-6017},
timestamp = {2010-02-05T11:28:48.000+0100},
title = {Glucocorticoids suppress tumor lymphangiogenesis of prostate cancer cells},
url = {PM:17062674},
volume = 12,
year = 2006
}