『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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EID=310071EID:310071, Map:0, LastModified:2016年4月19日(火) 15:36:04, Operator:[三好 小文], Avail:TRUE, Censor:0, Owner:[野間 隆文], 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): 国内共著 (徳島大学内研究者と国内(学外)研究者との共同研究 (国外研究者を含まない)) [継承]
学究種別 (推奨):
組織 (推奨):
著者 (必須): 1. (英) Koichi Fujisawa (日) (読)
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学籍番号 (推奨):
[継承]
2. (英) Shuji Terai (日) (読)
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学籍番号 (推奨):
[継承]
3. (英) Taro Takami (日) (読)
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学籍番号 (推奨):
[継承]
4. (英) Naoki Yamamoto (日) (読)
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学籍番号 (推奨):
[継承]
5. (英) Takahiro Yamasaki (日) (読)
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学籍番号 (推奨):
[継承]
6. (英) Toshihiko Matsumoto (日) (読)
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学籍番号 (推奨):
[継承]
7. (英) Kazuhito Yamaguch (日) (読)
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学籍番号 (推奨):
[継承]
8. (英) Yuji Owada (日) (読)
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学籍番号 (推奨):
[継承]
9. (英) Hiroshi Nishina (日) (読)
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学籍番号 (推奨):
[継承]
10.野間 隆文 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.分子医化学])
役割 (任意):
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学籍番号 (推奨):
[継承]
11. (英) Isao Sakaida (日) (読)
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貢献度 (任意):
学籍番号 (推奨):
[継承]
題名 (必須): (英) Modulation of anti-cancer drug sensitivity through the regulation of mitochondrial activity by adenylate kinase 4  (日)    [継承]
副題 (任意):
要約 (任意): (英) Background: Adenylate kinase is a key enzyme in the high-energy phosphoryl transfer reaction in living cells. Anisoform of this enzyme, adenylate kinase 4 (AK4), is localized in the mitochondrial matrix and is believed to beinvolved in stress, drug resistance, malignant transformation in cancer, and ATP regulation. However, the molecularbasis for the AK4 functions remained to be determined.Methods: HeLa cells were transiently transfected with an AK4 small interfering RNA (siRNA), an AK4 short hairpinRNA (shRNA) plasmid, a control shRNA plasmid, an AK4 expression vector, and a control expression vector toexamine the effect of the AK4 expression on cell proliferation, sensitivity to anti-cancer drug, metabolome, geneexpression, and mitochondrial activity.Results: AK4 knockdown cells treated with short hairpin RNA increased ATP production and showed greatersensitivity to hypoxia and anti-cancer drug, cis-diamminedichloro-platinum (II) (CDDP). Subcutaneous grafting AK4knockdown cells into nude mice revealed that the grafted cells exhibited both slower proliferation and reduced thetumor sizes in response to CDDP. AK4 knockdown cell showed a increased oxygen consumption rate with FCCPtreatment, while AK4 overexpression lowered it. Metabolome analysis showed the increased levels of thetricarboxylic acid cycle intermediates, fumarate and malate in AK4 knockdown cells, while AK4 overexpressionlowered them. Electron microscopy detected the increased mitochondrial numbers in AK4 knockdown cells.Microarray analysis detected the increased gene expression of two key enzymes in TCA cycle, succinatedehydrogenase A (SDHA) and oxoglutarate dehydrogenease L (OGDHL), which are components of SDH complexand OGDH complex, supporting the metabolomic results.Conclusions: We found that AK4 was involved in hypoxia tolerance, resistance to anti-tumor drug, and theregulation of mitochondrial activity. These findings provide a new potential target for efficient anticancer therapiesby controlling AK4 expression.  (日)    [継承]
キーワード (推奨): 1. (英) Adenylate kinase (日) (読) [継承]
2. (英) Drug resistance (日) (読) [継承]
3. (英) Energy metabolism (日) (読) [継承]
4. (英) Flux analysis (日) (読) [継承]
5. (英) Hypoxia (日) (読) [継承]
6. (英) Metabolome (日) (読) [継承]
7.ミトコンドリア (mitochondria) [継承]
発行所 (推奨):
誌名 (必須): Journal of Experimental & Clinical Cancer Research ([BioMed Central Ltd.])
(pISSN: 0392-9078, eISSN: 1756-9966)

ISSN (任意): 1756-9966
ISSN: 0392-9078 (pISSN: 0392-9078, eISSN: 1756-9966)
Title: Journal of experimental & clinical cancer research : CR
Title(ISO): J. Exp. Clin. Cancer Res.
Publisher: BioMed Central
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 35 [継承]
(必須): 1 [継承]
(必須): 48 48 [継承]
都市 (任意):
年月日 (必須): 西暦 2016年 3月 16日 (平成 28年 3月 16日) [継承]
URL (任意):
DOI (任意): 10.1186/s13046-016-0322-2    (→Scopusで検索) [継承]
PMID (任意): 26980435    (→Scopusで検索) [継承]
NAID (任意):
WOS (任意): 000372545600001 [継承]
Scopus (任意): 2-s2.0-84961201901 [継承]
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備考 (任意): 1.(英) Article.ELocationID: 10.1186/s13046-016-0322-2  (日)    [継承]
2.(英) Article.PublicationTypeList.PublicationType: Journal Article  (日)    [継承]
3.(英) OtherID: PMC4793738  (日)    [継承]
4.(英) KeywordList.Keyword: Adenylate kinase  (日)    [継承]
5.(英) KeywordList.Keyword: Drug resistance  (日)    [継承]
6.(英) KeywordList.Keyword: Energy metabolism  (日)    [継承]
7.(英) KeywordList.Keyword: Flux analysis  (日)    [継承]
8.(英) KeywordList.Keyword: Hypoxia  (日)    [継承]
9.(英) KeywordList.Keyword: Metabolome  (日)    [継承]
10.(英) KeywordList.Keyword: Mitochondria  (日)    [継承]

標準的な表示

和文冊子 ● Fujisawa Koichi, Terai Shuji, Takami Taro, Yamamoto Naoki, Yamasaki Takahiro, Matsumoto Toshihiko, Yamaguch Kazuhito, Owada Yuji, Nishina Hiroshi, Takafumi Noma and Sakaida Isao : Modulation of anti-cancer drug sensitivity through the regulation of mitochondrial activity by adenylate kinase 4, Journal of Experimental & Clinical Cancer Research, Vol.35, No.1, 48, 2016.
欧文冊子 ● Fujisawa Koichi, Terai Shuji, Takami Taro, Yamamoto Naoki, Yamasaki Takahiro, Matsumoto Toshihiko, Yamaguch Kazuhito, Owada Yuji, Nishina Hiroshi, Takafumi Noma and Sakaida Isao : Modulation of anti-cancer drug sensitivity through the regulation of mitochondrial activity by adenylate kinase 4, Journal of Experimental & Clinical Cancer Research, Vol.35, No.1, 48, 2016.

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