Item type |
デフォルトアイテムタイプ(フル)(1) |
公開日 |
2020-05-22 |
タイトル |
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タイトル |
Crucial role of carbonic anhydrase IX in tumorigenicity of xenotransplanted adult T-cell leukemia-derived cells |
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言語 |
en |
作成者 |
Nasu, Kentaro
Yamaguchi, Kazunori
Takanashi, Tomoka
Tamai, Keiichi
Sato, Ikuro
Ine, Shoji
Sasaki, Osamu
Satoh, Kennichi
Tanaka, Nobuyuki
Tanaka, Yuetsu
Fukushima, Takuya
Harigae, Hideo
Sugamura, Kazuo
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アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
権利情報 |
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言語 |
en |
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権利情報 |
Creative Commons Lisens Attribution-NonCommercial-NoDerivatives 4.0 |
権利情報 |
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言語 |
en |
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権利情報Resource |
https://creativecommons.org/licenses/by-nc-nd/4.0/ |
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権利情報 |
https://creativecommons.org/licenses/by-nc-nd/4.0/ |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
Adult T-cell leukemia/lymphoma |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
carbonic anhydrase IX |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
human T-cell leukemia virus type 1 |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
tumorigenicity |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
xenotransplantation |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
Carbonic anhydrase IX (CA9) is a membrane-associated carbonic anhydrase that regulates cellular pH, is upregulated in various solid tumors, and is considered to be a therapeutic target. Here, we describe the essential role of CA9 in the tumorigenicity of cells derived from human adult T-cell leukemia/lymphoma (ATL). We previously established the highly tumorigenic ST1-N6 subline from the ATL-derived ST1 cell line by serial xenotransplantation in NOG mice. In the present study, we first show that CA9 expression is strongly enhanced in ST1-N6 cells. We then sorted ST1 cells by high or low CA9 expression and established ST1-CA9(high) and ST1-CA9(low) sublines. ST1-CA9(high) cells, like ST1-N6 cells, were more strongly tumorigenic than ST1-CA9(low) or parental ST1 cells when injected into NOG mice. Knockdown of CA9 with shRNAs suppressed the ability of ST1-CA9(high) cells to initiate tumors, and the tumorigenicity of ST1 cells was significantly enhanced by introducing wild-type CA9 or a CA9 mutant with deletion of an intracytoplasmic domain. However, a CA9 with point mutations in the catalytic site did not increase the tumorigenicity of ST1 cells. Furthermore, we detected a small population of CA9(+)CD25(+) cells in lymph nodes of ATL patients. These findings suggest that CA9, and particularly its carbonic anhydrase activity, promotes the tumorigenicity of ATL-derived cells and may be involved in malignant development of lymphoma-type ATL. |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
論文 |
出版者 |
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言語 |
en |
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出版者 |
Wiley |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ |
journal article |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
出版タイプ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
識別子 |
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識別子 |
http://hdl.handle.net/20.500.12000/45871 |
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識別子タイプ |
HDL |
関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.1111/cas.13163 |
関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.1111/cas.13163 |
収録物識別子 |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
1349-7006 |
収録物名 |
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言語 |
en |
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収録物名 |
Cancer science |
書誌情報 |
巻 108,
号 3,
p. 435-443,
発行日 2017-03
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