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  1. 広島大学の刊行物
  2. Hiroshima Journal of Medical Sciences
  3. 49巻1号

Effects of N-(4-hydroxyphenyl) Retinamide on Urokinase-type Plasminogen Activator and Plasminogen Activator Inhibitor-1 in Prostate Adenocarcinoma Cell Lines

https://hiroshima.repo.nii.ac.jp/records/2013479
https://hiroshima.repo.nii.ac.jp/records/2013479
874de525-cf8d-4339-af28-1043714d2571
名前 / ファイル ライセンス アクション
HiroshimaJMedSci_49_67.pdf HiroshimaJMedSci_49_67.pdf (693.0 KB)
Item type デフォルトアイテムタイプ_(フル)(1)
公開日 2023-03-18
タイトル
タイトル Effects of N-(4-hydroxyphenyl) Retinamide on Urokinase-type Plasminogen Activator and Plasminogen Activator Inhibitor-1 in Prostate Adenocarcinoma Cell Lines
言語 en
作成者 Tanabe, Tetsuyuki

× Tanabe, Tetsuyuki

en Tanabe, Tetsuyuki

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アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
主題
主題Scheme Other
主題 Prostate cancer
主題
主題Scheme Other
主題 4-HPR
主題
主題Scheme Other
主題 uPA
主題
主題Scheme Other
主題 PAl-1
主題
主題Scheme NDC
主題 490
内容記述
内容記述 Previous investigations have demonstrated that a synthetic retinoid, N-(4-hydroxyphenyl) retinamide (4-HPR), inhibits the invasion of prostate adenocarcinoma in vitro. Urokinase-type plasminogen activator (uPA) is a prerequisite for tumor invasion. The purpose of this study was to evaluate the effects of 4-HPR on uPA and plasminogen activator inhibitor-1 (PAI-1) in prostate cancer.   Human prostate adenocacinoma cell lines, TSU-PR1 and PC3, were grown in serum-free media containing 4-HPR. Cellular mRNA and protein were subsequently extracted. Northern blot analysis, enzyme-linked immunosorbent assay (ELISA) and chromogenic functional analysis were performed on the samples.   Administration of 10-BM 4-HPR for 3 days resulted in an increase in uPA mRNA expression (TSU-PR1: 391 %, PC3: 356%), and a simultaneous increase in PAI-1 mRNA expression (TSUPR1: 217%, PC3: 235%) was observed. ELISA concomitantly demonstrated a significant increase (p<0.05) in uPA protein in the conditioned media (TSU-PR1: 134%, PC3: 139%) and cell lysates (TSU-PR1: 284%, PC3: 255%). Both cell lines demonstrated a significant increase (p<0.05) in PAI-1 protein in the conditioned media (TSU-PR1: 152%, PC3: 167%) and cell lysates (TSU-PR1: 170%, PC3: 222%). Concentrations below 10-sM failed to alter the protein production of either uPA or P AI-1. The functional uPA assay demonstrated a reduction of the proteolytic activity of uPA (TSU-PR1: 13%, PC3: 7%) in cell lysates of 10-BM 4-HPR (p<0.05), while there was minimal uPA activity in the conditioned media.   4-HPR stimulates a paradoxical increase in uPA and PAI-1, but the anti-invasive effects of 4-HPR are consistent with the increase in both uPA and PAI-1, resulting in an overall reduction of functional uPA activities.
言語 en
出版者
出版者 Hiroshima University Medical Press
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ departmental bulletin paper
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 0018-2052
収録物識別子
収録物識別子タイプ NCID
収録物識別子 AA00664312
開始ページ
開始ページ 67
書誌情報 Hiroshima Journal of Medical Sciences
Hiroshima Journal of Medical Sciences

巻 49, 号 1, p. 67-72, 発行日 2000-03
旧ID 37703
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