Item type |
文献 / Documents(1) |
公開日 |
2025-03-18 |
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 |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
出版社版DOI |
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関連識別子 |
https://doi.org/10.1016/j.celrep.2023.112479 |
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関連名称 |
10.1016/j.celrep.2023.112479 |
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 |
タイトル |
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タイトル |
p53-independent tumor suppression by cell-cycle arrest via CREB/ATF transcription factor OASIS |
著者 |
Saito, Atsushi
Kamikawa, Yasunao
Ito, Taichi
Matsuhisa, Koji
Kaneko, Masayuki
Okamoto, Takumi
吉丸, 哲郎
松下, 洋輔
片桐, 豊雅
Imaizumi, Kazunori
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抄録 |
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内容記述 |
CREB/ATF transcription factor OASIS/CREB3L1 is upregulated in long-term-cultured astrocytes undergoing cell-cycle arrest due to loss of DNA integrity by repeated replication. However, the roles of OASIS in the cell cycle remain unexplored. We find that OASIS arrests the cell cycle at G2/M phase after DNA damage via direct induction of p21. Cell-cycle arrest by OASIS is dominant in astrocytes and osteoblasts, but not in fibroblasts, which are dependent on p53. In a brain injury model, Oasis−/− reactive astrocytes surrounding the lesion core show sustained growth and inhibition of cell-cycle arrest, resulting in prolonged gliosis. We find that some glioma patients exhibit low expression of OASIS due to high methylation of its promoter. Specific removal of this hypermethylation in glioblastomas transplanted into nude mice by epigenomic engineering suppresses the tumorigenesis. These findings suggest OASIS as a critical cell-cycle inhibitor with potential to act as a tumor suppressor. |
書誌情報 |
en : Cell Reports
巻 42,
号 5,
p. 112479,
発行日 2023-05-30
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収録物ID |
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収録物識別子タイプ |
EISSN |
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収録物識別子 |
22111247 |
出版者 |
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出版者 |
Elsevier |
権利情報 |
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権利情報 |
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
EID |
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識別子 |
413227 |
言語 |
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言語 |
eng |