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著作: Kashiwakura Yuji/[落合 和彦]/Watanabe Masami/Abarzua Fernando/Sakaguchi Masakiyo/Takaoka Munenori/Tanimoto Ryuta/Nasu Yasutomo/Huh Nam-Ho/Kumon Hiromi/Down-regulation of inhibition of differentiation-1 via activation of activating transcription factor 3 and Smad regulates REIC/Dickkopf-3-induced apoptosis./[Cancer Research]

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EID
210013
EOID
654233
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LastModified
2012年8月28日(火) 21:39:00
Operator
大家 隆弘
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TRUE
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[副研究部長]/[徳島大学.大学院ヘルスバイオサイエンス研究部]
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種別 必須 学術論文(審査論文)
言語 必須 英語
招待 推奨
審査 推奨
カテゴリ 推奨
共著種別 推奨
学究種別 推奨
組織 推奨
著者 必須
  1. (英) Kashiwakura Yuji
    役割 任意
    貢献度 任意
    学籍番号 推奨
  2. 落合 和彦
    役割 任意
    貢献度 任意
    学籍番号 推奨
  3. (英) Watanabe Masami
    役割 任意
    貢献度 任意
    学籍番号 推奨
  4. (英) Abarzua Fernando
    役割 任意
    貢献度 任意
    学籍番号 推奨
  5. (英) Sakaguchi Masakiyo
    役割 任意
    貢献度 任意
    学籍番号 推奨
  6. (英) Takaoka Munenori
    役割 任意
    貢献度 任意
    学籍番号 推奨
  7. (英) Tanimoto Ryuta
    役割 任意
    貢献度 任意
    学籍番号 推奨
  8. (英) Nasu Yasutomo
    役割 任意
    貢献度 任意
    学籍番号 推奨
  9. (英) Huh Nam-Ho
    役割 任意
    貢献度 任意
    学籍番号 推奨
  10. (英) Kumon Hiromi
    役割 任意
    貢献度 任意
    学籍番号 推奨
題名 必須

(英) Down-regulation of inhibition of differentiation-1 via activation of activating transcription factor 3 and Smad regulates REIC/Dickkopf-3-induced apoptosis.

副題 任意
要約 任意

(英) REIC/Dickkopf-3 (Dkk-3), a tumor suppressor gene, has been investigated in gene therapy studies. Our previous study suggested that REIC/Dkk-3-induced apoptosis mainly resulted from phosphorylation of c-Jun-NH(2) kinase (JNK) in prostate cancer cells. However, the precise mechanisms, especially the molecular mechanisms regulating JNK phosphorylation, remain unclear. In this study, we investigated the mechanisms participating in JNK phosphorylation in the context of a refractory cancer disease, malignant mesothelioma (MM). Adenovirus-mediated overexpression of REIC/Dkk-3 induced apoptosis mainly through JNK activation in immortalized MM cells (211H cells). Interestingly, transcriptional down-regulation of inhibition of differentiation-1 (Id-1) was detected in REIC/Dkk-3-overexpressed 211H cells. Moreover, restoration of Id-1 expression antagonized REIC/Dkk-3-induced JNK phosphorylation and apoptosis. Mutagenesis experiments with the 2.1-kb human Id-1 promoter revealed that activating transcription factor 3 (ATF3) and Smad interaction, with their respective binding motifs, was essential for REIC/Dkk-3-mediated suppression of Id-1 promoter activity. ATF3 activation was probably induced by endoplasmic reticulum stress. Finally, we showed strong antitumor effects from REIC/Dkk-3 gene transfer into the pleural cavity in an orthotopic MM mouse model. Relative to control tumor tissue, REIC/Dkk-3-treated tumor tissue showed down-regulated expression of Id-1 mRNA, enhanced expression of phosphorylated JNK, and an increased number of apoptotic cells. In summary, we first showed that both ATF3 and Smad were crucially and synergistically involved in down-regulation of Id-1, which regulated JNK phosphorylation in REIC/Dkk-3-induced apoptosis. Thus, gene therapy with REIC/Dkk-3 may be a promising therapeutic tool for MM.

キーワード 推奨
  1. (英) Activating Transcription Factor 3
  2. (英) Animals
  3. アポトーシス(apoptosis)
  4. (英) Down-Regulation
  5. 小胞体(endoplasmic reticulum)
  6. 遺伝子治療(gene therapy)
  7. (英) Hela Cells
  8. (英) Humans
  9. (英) Inhibitor of Differentiation Protein 1
  10. (英) Intercellular Signaling Peptides and Proteins
  11. (英) JNK Mitogen-Activated Protein Kinases
  12. (英) Mice
  13. (英) Mice, Inbred BALB C
  14. (英) Multiple Myeloma
  15. (英) NF-kappa B
  16. リン酸化(phosphorylation)
  17. (英) Promoter Regions, Genetic
  18. (英) Smad Proteins
発行所 推奨
誌名 必須 Cancer Research(American Assotiation for Cancer Research)
(pISSN: 0008-5472, eISSN: 1538-7445)
ISSN 任意 1538-7445
ISSN: 0008-5472 (pISSN: 0008-5472, eISSN: 1538-7445)
Title: Cancer research
Title(ISO): Cancer Res
Publisher: American Association for Cancer Research
 (NLM Catalog  (Scopus  (Scopus  (Scopus  (CrossRef (Scopus information is found. [need login])
必須 68
必須 20
必須 8333 8341
都市 任意
年月日 必須 2008年 10月 15日
URL 任意
DOI 任意 10.1158/0008-5472.CAN-08-0080    (→Scopusで検索)
PMID 任意 18922905    (→Scopusで検索)
NAID 任意
WOS 任意
Scopus 任意
評価値 任意
被引用数 任意
指導教員 推奨
備考 任意
  1. (英) Article.Affiliation: Innovation Center Okayama for Nanobio-Targeted Therapy, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. yu-kashi@cj9.so-net.ne.jp

  2. (英) Article.PublicationTypeList.PublicationType: Journal Article

  3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't