『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
ID: Pass:

登録内容 (EID=316894)

EID=316894EID:316894, Map:0, LastModified:2019年3月2日(土) 20:42:08, Operator:[[ADMIN]], Avail:TRUE, Censor:承認済, Owner:[片桐 豊雅], Read:継承, Write:継承, Delete:継承.
種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
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) Nakamura Toru (日) (読)
役割 (任意):
貢献度 (任意):
学籍番号 (推奨):
[継承]
2.片桐 豊雅
役割 (任意):
貢献度 (任意):
学籍番号 (推奨):
[継承]
3. (英) Sato Shoki (日) (読)
役割 (任意):
貢献度 (任意):
学籍番号 (推奨):
[継承]
4. (英) Kushibiki Toshihiro (日) (読)
役割 (任意):
貢献度 (任意):
学籍番号 (推奨):
[継承]
5. (英) Hontani Koji (日) (読)
役割 (任意):
貢献度 (任意):
学籍番号 (推奨):
[継承]
6. (英) Tsuchikawa Takahiro (日) (読)
役割 (任意):
貢献度 (任意):
学籍番号 (推奨):
[継承]
7. (英) Hirano Satoshi (日) (読)
役割 (任意):
貢献度 (任意):
学籍番号 (推奨):
[継承]
8. (英) Nakamura Yusuke (日) (読)
役割 (任意):
貢献度 (任意):
学籍番号 (推奨):
[継承]
題名 (必須): (英) Overexpression of C16orf74 is involved in aggressive pancreatic cancers.  (日)    [継承]
副題 (任意):
要約 (任意): (英) Clinical outcome of pancreatic ductal adenocarcinoma (PDAC) has not been improved in the last three decades due to the lack of effective molecular-targeted drugs. To identify a novel therapeutic target for PDAC, we have performed genome-wide anamysis and found that Homo sapiens chromosome 16 open reading frame 74 (C16orf74) was up-regulated in the vast majority of PDAC. Overexpression of C16orf74protein detected by immunohistochemical analysis was an independent prognostic factor for patients with PDAC. The knockdown of endogenous C16orf74 expression in the PDAC cell lines KLM-1 and PK-59 by vector-based small hairpin-RNA (shRNA) drastically attenuated the growth of those cells, whereas ectopic C16orf74 overexpression in HEK293T and NIH3T3 cells promoted cell growth and invasion, respectively. More importantly, the endogenous threonine 44 (T44)-phosphorylated form of C16orf74 interacted with the protein phosphatase 3 catalytic subunit alpha (PPP3CA) via the PDIIIT sequence in the PPP3CA-binding motif within the middle portion of C16orf74 in PDAC cells. The overexpression of mutants of C16orf74 lacking the PDIIIT sequence or T44 phosphorylation resulted in the suppression of invasive activity compared with wild-type C16orf74, indicating that their interaction should be indispensable for PDAC cell invasion. These results suggest that C16orf74 plays an important role for PDAC invasion and proliferation, and is a promising target for a specific treatment for patients with PDAC.  (日)    [継承]
キーワード (推奨):
発行所 (推奨):
誌名 (必須): Oncotarget (Impact Journals)
(eISSN: 1949-2553)

ISSN (任意): 1949-2553
ISSN: 1949-2553 (eISSN: 1949-2553)
Title: Oncotarget
Title(ISO): Oncotarget
Publisher: Impact Journals LLC
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
[継承]
[継承]
(必須): 8 [継承]
(必須): 31 [継承]
(必須): 50460 50475 [継承]
都市 (任意):
年月日 (必須): 西暦 2016年 7月 28日 (平成 28年 7月 28日) [継承]
URL (任意):
DOI (任意): 10.18632/oncotarget.10912    (→Scopusで検索) [継承]
PMID (任意): 28881575    (→Scopusで検索) [継承]
CRID (任意):
Scopus (任意):
機関リポジトリ : 113051 [継承]
researchmap (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) PublicationType: JOURNAL ARTICLE  (日)    [継承]

標準的な表示

和文冊子 ● Toru Nakamura, Toyomasa Katagiri, Shoki Sato, Toshihiro Kushibiki, Koji Hontani, Takahiro Tsuchikawa, Satoshi Hirano and Yusuke Nakamura : Overexpression of C16orf74 is involved in aggressive pancreatic cancers., Oncotarget, 8, 31, 50460-50475, 2016.
欧文冊子 ● Toru Nakamura, Toyomasa Katagiri, Shoki Sato, Toshihiro Kushibiki, Koji Hontani, Takahiro Tsuchikawa, Satoshi Hirano and Yusuke Nakamura : Overexpression of C16orf74 is involved in aggressive pancreatic cancers., Oncotarget, 8, 31, 50460-50475, 2016.

関連情報

Number of session users = 2, LA = 2.63, Max(EID) = 467923, Max(EOID) = 1243747.