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Oncogenic fusion gene CD74-NRG1 confers cancer stem cell-like properties in lung cancer through a IGF2 autocrine/paracrine circuit
http://hdl.handle.net/2297/44818
http://hdl.handle.net/2297/44818bba7d8a7-28e5-4b3c-aa88-8603ef9a362e
名前 / ファイル | ライセンス | アクション |
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CA-PR-GOTOH-N-974.pdf (844.1 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-05 | |||||
タイトル | ||||||
タイトル | Oncogenic fusion gene CD74-NRG1 confers cancer stem cell-like properties in lung cancer through a IGF2 autocrine/paracrine circuit | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Murayama, Takahiko
× Murayama, Takahiko× Nakaoku, Takashi× Enari, Masato× Nishimura, Tatsunori× Tominaga, Kana× Nakata, Asuka× Tojo, Arinobu× Sugano, Sumio× Kohno, Takashi× Gotoh, Noriko |
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書誌情報 |
Cancer Research 巻 76, 号 4, p. 974-983, 発行日 2016-02-15 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0008-5472 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA12059243 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1158/0008-5472.CAN-15-2135 | |||||
出版者 | ||||||
出版者 | American Association for Cancer Research Inc. | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | The CD74-Neuregulin1 (NRG1) fusion gene was recently identified as novel driver of invasive mucinous adenocarcinoma, a malignant form of lung cancer. However, the function of the CD74-NRG1 fusion gene in adenocarcinoma pathogenesis and the mechanisms by which it may impart protumorigenic characteristics to cancer stem cells (CSC) is still unclear. In this study, we found that the expression of the CD74-NRG1 fusion gene increased the population of lung cancer cells with CSC-like properties. CD74-NRG1 expression facilitated sphere formation not only of cancer cells, but also of nonmalignant lung epithelial cells. Using a limiting dilution assay in a xenograft model, we further show that the CD74-NRG1 fusion gene enhanced tumor initiation. Mechanistically, we found that CD74-NRG1 expression promoted the phosphorylation of ErbB2/3 and activated the PI3K/Akt/NF-κB signaling pathway. Furthermore, the expression of the secreted insulin-like growth factor 2 (IGF2) and phosphorylation of its receptor, IGF1R, were enhanced in an NF-κB-dependent manner in cells expressing CD74-NRG1. These findings suggest that CD74-NRG1-induced NF-κB activity promotes the IGF2 autocrine/paracrine circuit. Moreover, inhibition of ErbB2, PI3K, NF-κB, or IGF2 suppressed CD74-NRG1-induced tumor sphere formation. Therefore, our study provides a preclinical rationale for developing treatment approaches based on these identified pathways to suppress CSC properties that promote tumor progression and recurrence. © 2016 American Association for Cancer Research. | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa |