A DDX31/mutant-p53/EGFR axis promotes multistep progression of muscle invasive bladder cancer

• Material Type: 博士論文
• Title: A DDX31/mutant-p53/EGFR axis promotes multistep progression of muscle invasive bladder cancer
• Author/Editor: Daizumoto, Kei; Yoshimaru, Tetsuro; Matsushita, Yosuke; Fukawa, Tomoya; Uehara, Hisanori; Ono, Masaya; Komatsu, Masato; Kanayama, Hiro-omi; Katagiri, Toyomasa
• Author Heading: Daizumoto, Kei; Yoshimaru, Tetsuro; Matsushita, Yosuke; Fukawa, Tomoya; Uehara, Hisanori; Ono, Masaya; Komatsu, Masato; Kanayama, Hiro-omi; Katagiri, Toyomasa
• Publication, Distribution, etc.: American Association for Cancer Research
• Publication Date: 2018-02-13
• Publication Date (W3CDTF): 2018-02-13
• Alternative Title: DDX31/p53変異/EGFR経路は筋層浸潤膀胱癌の多段階進展を促進する; Critical roles of DDX31-mutp53-EGFR axis in MIBC progression
• Periodical title: Cancer Research
• No. or year of volume/issue: 78 9
• Volume: 78
• Issue: 9
• Pages: 2233-2247
• ISSN (Periodical Title): ISSN : 0008-5472; ISSN : 1538-7445
• Degree grantor/type: 徳島大学
• Date Granted: 2018-04-26
• Dissertation Number: 甲第3194号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: DDX31; mutant-p53; EGFR; muscle invasive bladder cancer
• Target Audience: 一般
• Note (General): The p53 and EGFR pathways are frequently altered in bladder cancers, yet their contributions to its progression remain elusive. Here we report that DEAD box polypeptide 31 (DDX31) plays a critical role in the multistep progression of muscle invasive bladder cancer (MIBC) through its sequential interactions with mutant p53 (mutp53) and EGFR. In early MIBC cells, nuclear DDX31 bound mutp53/SP1 and enhanced mutp53 transcriptional activation, leading to migration and invasion of MIBC. Cytoplasmic DDX31 also bound EGFR and phospho-nucleolin (p-NCL) in advanced MIBC, leading to EGFR-Akt signaling activation. High expression of both cytoplasmic DDX31 and p53 proteins correlated with poor prognosis in patients with MIBC, and blocking the DDX31-NCL interaction resulted in downregulation of EGFR-Akt signaling, eliciting an in vivo anti-tumor effect against bladder cancer. These findings reveal that DDX31 cooperates with mutp53 and EGFR to promote progression of MIBC, and inhibition of DDX31-NCL formation may lead to potential treatment strategies for advanced MIBC.
• Format (IMT): application/pdf
• Access Restrictions: インターネット公開
• Related Material (DOI): 10.1158/0008-5472.CAN-17-2528
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 徳島大学 : 徳島大学機関リポジトリ

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