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  1. H-1. がん進展制御研究所
  2. h-1 10. 学術雑誌掲載論文
  3. 1. 査読済論文

Critical role of glioma-associated oncogene homolog 1 in maintaining invasive and mesenchymal-like properties of melanoma cells

https://doi.org/10.24517/00027520
https://doi.org/10.24517/00027520
79e4ca29-0125-4486-8624-fac8963b543f
名前 / ファイル ライセンス アクション
CA-PR-YOSHIOKA-K-1602.pdf CA-PR-YOSHIOKA-K-1602.pdf (1.6 MB)
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Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-10-05
タイトル
タイトル Critical role of glioma-associated oncogene homolog 1 in maintaining invasive and mesenchymal-like properties of melanoma cells
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
ID登録
ID登録 10.24517/00027520
ID登録タイプ JaLC
著者 Gunarta, I Ketut

× Gunarta, I Ketut

WEKO 48013

Gunarta, I Ketut

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Li, Rong

× Li, Rong

WEKO 48014

Li, Rong

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Nakazato, Ryota

× Nakazato, Ryota

WEKO 47932
金沢大学研究者情報 30761803
研究者番号 30761803

Nakazato, Ryota

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Suzuki, Ryusuke

× Suzuki, Ryusuke

WEKO 48015

Suzuki, Ryusuke

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Boldbaatar, Jambaldorj

× Boldbaatar, Jambaldorj

WEKO 48016

Boldbaatar, Jambaldorj

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Suzuki, Takeshi

× Suzuki, Takeshi

WEKO 183
e-Rad 30262075
研究者番号 30262075

Suzuki, Takeshi

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Yoshioka, Katsuji

× Yoshioka, Katsuji

WEKO 142
e-Rad 60200937
金沢大学研究者情報 60200937
研究者番号 60200937

Yoshioka, Katsuji

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著者別表示 中里, 亮太

× 中里, 亮太

中里, 亮太

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鈴木, 健之

× 鈴木, 健之

鈴木, 健之

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善岡, 克次

× 善岡, 克次

善岡, 克次

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書誌情報 Cancer Science

巻 108, 号 8, p. 1602-1611, 発行日 2017-08-01
ISSN
収録物識別子タイプ ISSN
収録物識別子 1347-9032
NCID
収録物識別子タイプ NCID
収録物識別子 AA11808050
DOI
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 10.1111/cas.13294
出版者
出版者 Japanese Cancer Association = 日本癌学会/ Blackwell Publishing Ltd
抄録
内容記述タイプ Abstract
内容記述 Cutaneous melanoma is the most aggressive form of skin cancer. This aggressiveness appears to be due to the cancer cells' ability to reversibly switch between phenotypes with non-invasive and invasive potential, and microphthalmia-associated transcription factor (MITF) is known to play a central role in this process. The transcription factor glioma-associated oncogene homolog 1 (GLI1) is a component of the canonical and noncanonical sonic hedgehog pathways. Although GLI1 has been suggested to be involved in melanoma progression, its precise role and the mechanism underlying invasion remain unclear. Here we investigated whether and how GLI1 is involved in the invasive ability of melanoma cells. Gli1 knockdown (KD) melanoma cell lines, established by using Gli1-targeting lentiviral short hairpin RNA, exhibited a markedly reduced invasion ability, but their MITF expression and activity were the same as controls. Gli1 KD melanoma cells also led to less lung metastasis in mice compared with control melanoma cells. Furthermore, the Gli1 KD melanoma cells underwent a mesenchymal-to-epithelial-like transition, accompanied by downregulation of the epithelial-to-mesenchymal transition (EMT)-inducing transcription factors (EMT-TF) Snail1, Zeb1 and Twist1, but not Snail2 or Zeb2. Collectively, these results indicate that GLI1 is important for maintaining the invasive and mesenchymal-like properties of melanoma cells independent of MITF, most likely by modulating a subset of EMT-TF. Our findings provide new insight into how heterogeneity and plasticity are achieved and regulated in melanoma. © 2017 Japanese Cancer Association.
権利
権利情報 Copyright © 2017 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. | The definitive version is available at http://onlinelibrary.wiley.com/doi/10.1111/cas.13294 (CC-BY NC ND)
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
関連URI
識別子タイプ URI
関連識別子 http://onlinelibrary.wiley.com/doi/10.1111/cas.13294
関連URI
識別子タイプ URI
関連識別子 http://www.jca.gr.jp/
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