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Elevated β-catenin pathway as a novel target for patients with resistance to EGF receptor targeting drugs
http://hdl.handle.net/2297/45447
http://hdl.handle.net/2297/45447230d423a-985f-48d1-a65e-5943332aaac3
名前 / ファイル | ライセンス | アクション |
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CA-PR-GOTO-N-13076.pdf (659.8 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 | Elevated β-catenin pathway as a novel target for patients with resistance to EGF receptor targeting drugs | |||||
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 |
Nakata, Asuka
× Nakata, Asuka× Yoshida, Ryo× Yamaguchi, Rui× Yamauchi, Mai× Tamada, Yoshinori× Fujita, Andre× Shimamura, Teppei× Imoto, Seiya× Higuchi, Tomoyuki× Nomura, Masaharu× Kimura, Tatsuo× Nokihara, Hiroshi× Higashiyama, Masahiko× Kondoh, Kazuya× Nishihara, Hiroshi× Tojo, Arinobu× Yano, Seiji× Miyano, Satoru× Gotoh, Noriko |
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書誌情報 |
Scientific Reports 巻 5, p. 13076, 発行日 2015-08-13 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 2045-2322 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1038/srep13076 | |||||
出版者 | ||||||
出版者 | Nature Publishing Group | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | There is a high death rate of lung cancer patients. Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are effective in some lung adenocarcinoma patients with EGFR mutations. However, a significant number of patients show primary and acquire resistance to EGFR-TKIs. Although the Akt kinase is commonly activated due to various resistance mechanisms, the key targets of Akt remain unclear. Here, we show that the Akt-β-catenin pathway may be a common resistance mechanism. We analyzed gene expression profiles of gefitinib-resistant PC9M2 cells that were derived from gefitinib-sensitive lung cancer PC9 cells and do not have known resistance mechanisms including EGFR mutation T790M. We found increased expression of Axin, a β-catenin target gene, increased phosphorylation of Akt and GSK3, accumulation of β-catenin in the cytoplasm/nucleus in PC9M2 cells. Both knockdown of β-catenin and treatment with a β-catenin inhibitor at least partially restored gefitinib sensitivity to PC9M2 cells. Lung adenocarcinoma tissues derived from gefitinib-resistant patients displayed a tendency to accumulate β-catenin in the cytoplasm. We provide a rationale for combination therapy that includes targeting of the Akt-β-catenin pathway to improve the efficacy of EGFR-TKIs. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |