%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 }