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Hypoxia-independent overexpression of hypoxia-inducible factor 1α as an early change in mouse hepatocarcinogenesis.
https://asahikawa-med.repo.nii.ac.jp/records/1526
https://asahikawa-med.repo.nii.ac.jp/records/152656abb8a1-7d52-434e-941f-05849a8f54cd
名前 / ファイル | ライセンス | アクション |
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Item type | 学術雑誌論文 / Journal Article_02(1) | |||||||||||||||||||||||||||
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公開日 | 2009-04-24 | |||||||||||||||||||||||||||
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タイトル | Hypoxia-independent overexpression of hypoxia-inducible factor 1α as an early change in mouse hepatocarcinogenesis. | |||||||||||||||||||||||||||
言語 | en | |||||||||||||||||||||||||||
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言語 | eng | |||||||||||||||||||||||||||
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資源タイプ | journal article | |||||||||||||||||||||||||||
その他(別言語等)のタイトル | ||||||||||||||||||||||||||||
その他のタイトル | Hypoxia-independent overexpression of HIF-1α as an early change in mouse hepatocarcinogenesis. | |||||||||||||||||||||||||||
言語 | en | |||||||||||||||||||||||||||
著者 |
田中, 宏樹
× 田中, 宏樹
× Yamamoto, M
× Hashimoto, N
× Miyakoshi, M
× Tamakawa, S
× Yoshie, M
× Tokusashi, Y
× Yokoyama, K
× Yaginuma, Y
× Ogawa, K
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著者 ローマ字 | ||||||||||||||||||||||||||||
Tanaka, Hiroki | ||||||||||||||||||||||||||||
著者 ローマ字 | ||||||||||||||||||||||||||||
en | ||||||||||||||||||||||||||||
書誌情報 |
Cancer Research 巻 66, 号 23, p. 11263-11270, 発行日 2006-12-01 |
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収録物識別子タイプ | ISSN | |||||||||||||||||||||||||||
収録物識別子 | 0008-5472 | |||||||||||||||||||||||||||
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関連タイプ | isVersionOf | |||||||||||||||||||||||||||
識別子タイプ | DOI | |||||||||||||||||||||||||||
関連識別子 | 10.1158/0008-5472.CAN-06-1699 | |||||||||||||||||||||||||||
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内容記述タイプ | Other | |||||||||||||||||||||||||||
内容記述 | http://dx.doi.org/10.1158/0008-5472.CAN-06-1699 | http://dx.doi.org/10.1158/0008-5472.CAN-06-1699 | |||||||||||||||||||||||||||
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内容記述タイプ | Abstract | |||||||||||||||||||||||||||
内容記述 | HIF-1 is involved in tumor progression/metastasis and activated in various cancers. Here we show that HIF-1α, which plays a major role in HIF-1 activation, is over-expressed in preneoplastic hepatocytic lesions from a very early stage during hepatocarcinogenesis in mice and man. Transcriptional targets of HIF-1, such as VEGF, glut-1, c-met and Igf-2, were also over-expressed in mice lesions. HIF-1α expression was independent of hypoxia, because pimonidazole immunostaining was negative in the mouse lesions after treatment with pimonidazole. On the other hand, Akt, the pathway of which can up-regulate HIF-1α expression, was activated in the mouse lesions, while HIF-1α was markedly downregulated in the mouse HCC cell lines after treatment with a PI3 kinase (PI3K) inhibitor, LY294002, indicating that HIF-1α expression is dependent on PI3K/Akt signaling. Conversely, HIF-1α knockdown by siRNA in the HCC cell line resulted in decreased expression of activated Akt together with the HIF-1 target genes, indicating that Akt activation is reversely dependent on HIF-1 activation. Treating the HCC cells with Igf-2 upregulated both phospho-Akt and HIF-1α, while inhibition of Igf-2 by the neutralizing Igf-2 antibody downregulated them both, suggesting that Igf-2 may, at least in part, mediate the activation of Akt and HIF-1α. However, Akt was not activated by Igf-2 or EGF in the HIF-1α knockdown cells, indicating that expression of the HIF-1 target genesis necessary for the Akt activation. These findings suggest that the reciprocal activation of PI3K/Akt signaling and HIF-1α may be important in progression of hepatocarcinogenesis. | |||||||||||||||||||||||||||
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内容記述タイプ | Other | |||||||||||||||||||||||||||
注記 | author | |||||||||||||||||||||||||||
言語 | en | |||||||||||||||||||||||||||
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内容記述タイプ | Other | |||||||||||||||||||||||||||
資源タイプ | text | |||||||||||||||||||||||||||
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出版タイプ | AM | |||||||||||||||||||||||||||
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内容記述タイプ | Other | |||||||||||||||||||||||||||
内容記述 | application/pdf | |||||||||||||||||||||||||||
ID(XooNIps) | ||||||||||||||||||||||||||||
17145871 | ||||||||||||||||||||||||||||
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1110 |