Down-regulation of MDR1 by Ad-DKK3 via Akt/NFκB pathways augments the anti-tumor effect of temozolomide in glioblastoma cells and a murine xenograft model 2

• 資料種別: 博士論文
• ISSN: 0167-594X
• タイトル: Down-regulation of MDR1 by Ad-DKK3 via Akt/NFκB pathways augments the anti-tumor effect of temozolomide in glioblastoma cells and a murine xenograft model
• 巻次・部編番号: 139 2
• 著者・編者: Fujihara, Toshitaka; Mizobuchi, Yoshifumi; Nakajima, Kohei; Kageji, Teruyoshi; Matsuzaki, Kazuhito; Kitazato, Keiko T.; Otsuka, Ryotaro; Hara, Keijiro; Mure, Hideo; Okazaki, Toshiyuki; Kuwayama, Kazuyuki; Nagahiro, Shinji; Takagi, Yasushi
• 著者標目: Fujihara, Toshitaka; Mizobuchi, Yoshifumi; Nakajima, Kohei; Kageji, Teruyoshi; Matsuzaki, Kazuhito; Kitazato, Keiko T.; Otsuka, Ryotaro; Hara, Keijiro; Mure, Hideo; Okazaki, Toshiyuki; Kuwayama, Kazuyuki; Nagahiro, Shinji; Takagi, Yasushi
• 出版事項: Springer Science+Business Media, LLC
• 出版年月日等: 2018-05-19
• 出版年（W3CDTF）: 2018-05-19
• 並列タイトル等: 膠芽腫細胞およびマウス背部皮下モデルにおいて，アデノウイルスベクターを用いたDKK3の導入はAkt/NFκB経路を介してMDR1の発現を抑制し，テモゾロミドによる抗腫瘍効果を増強する
• タイトル（掲載誌）: Journal of Neuro-Oncology
• 授与機関名: 徳島大学
• 授与年月日: 2018-10-25
• 授与年月日（W3CDTF）: 2018-10-25
• 報告番号: 甲第3239号
• 学位: 博士（医学）
• 博論授与番号: 甲第3239号
• 本文の言語コード: eng
• 件名標目: DKK3; MDR1; Akt; glioblastoma; temozolomide
• 対象利用者: 一般
• 一般注記: Background: Glioblastoma multiforme (GBM) is the most malignant of brain tumors. Acquired drug resistance is a major obstacle for successful treatment. Earlier studies reported that expression of the multiple drug resistance gene (MDR1) is regulated by YB-1 or NFκB via the JNK/c-Jun or Akt pathway. Over-expression of the Dickkopf (DKK) family member DKK3 by an adenovirus vector carrying DKK3 (Ad-DKK3) exerted anti-tumor effects and led to the activation of the JNK/c-Jun pathway. We investigated whether Ad-DKK3 augments the anti-tumor effect of temozolomide (TMZ) via the regulation of MDR1.Methods: GBM cells (U87MG and U251MG), primary TGB105 cells, and mice xenografted with U87MG cells were treated with Ad-DKK3 or TMZ alone or in combination.Results: Ad-DKK3 augmentation of the anti-tumor effects of TMZ was associated with reduced MDR1 expression in both in vivo and in vitro studies. The survival of Ad-DKK3-treated U87MG cells was inhibited and the expression of MDR1 was reduced. This was associated with the inhibition of Akt/NFκB but not of YB-1 via the JNK/c-Jun- or Akt pathway.Conclusions: Our results suggest that Ad-DKK3 regulates the expression of MDR1 via Akt/NFκB pathways and that it augments the anti-tumor effects of TMZ in GBM cells.
• DOI: info:doi/10.1007/s11060-018-2894-5; https://doi.org/info:doi/10.1007/s11060-018-2894-5
• 国立国会図書館永続的識別子: info:ndljp/pid/11671792; https://dl.ndl.go.jp/pid/11671792
• コレクション（共通）: 障害者向け資料
• コレクション（障害者向け資料：レベル1）: テキストデータ
• コレクション（個別）: 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• 収集根拠: 博士論文（自動収集）
• 受理日（W3CDTF）: 2021-05-16T23:51:55+09:00
• 記録形式（IMT）: application/pdf
• オンライン閲覧公開範囲: 国立国会図書館内限定公開
• デジタル化資料送信: 図書館・個人送信対象外
• 遠隔複写可否（NDL）: 可
• 掲載誌（URI）: http://repo.lib.tokushima-u.ac.jp/112895
• 連携機関・データベース: 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp