| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2023-02-18 |
| タイトル |
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|
タイトル |
Downregulation of miR-26 promotes invasion and metastasis via targeting interleukin-22 in cutaneous T-cell lymphoma |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
CTCL |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
cutaneous T-cell lymphoma |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
IL-22 |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
\ninterleukin-22 |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
miR-26 |
| 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 |
| アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 作成者 |
Matsuda, Yuka
Ikeda, Sho
Abe, Fumito
Takahashi, Yuto
Kitadate, Akihiro
Takahashi, Naoto
Wakui, Hideki
Tagawa, Hiroyuki
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| 内容記述 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
It has been reported that certain microRNAs (miRNA) are associated with the pathogenesis of lymphoma. We have previously demonstrated that histone deacetylase inhibitors restore tumor-suppressive miRNAs, such as miR-16, miR-29, miR-150, and miR-26, in advanced cutaneous T-cell lymphoma (CTCL). Among these, the function of miR-26 remains unclear. In this study, we aimed to reveal the function of miR-26 in CTCL oncogenesis. First, we confirmed that the miR-26 family was markedly dysregulated in CTCL cell lines and primary samples. In vivo analysis using miR-26a-transduced CTCL cells injected into immunodeficient NOG mice demonstrated the significant prolonged survival of the mice, suggesting that the miRNA had a tumor-suppressive function. We performed gene expression assays and identified 12 candidate miR-26 targets, namely RGS13, FAM71F1, OAF, SNX21, CDH2, PTPLB, IL22, DNAJB5, CASZ1, CACNA1C, MYH10, and CNR1. Among these, IL22 was the most likely candidate target because the IL-22–STAT3–CCL20–CCR6 cascade is associated with tumor invasion and metastasis of advanced CTCL. In vitro analysis of IL22 and IL22RA knockdown and miR-26 transduction demonstrated inhibited CTCL cell migration. In particular, IL22 knockdown induced cell apoptosis. Finally, we conducted in vivo inoculation analysis of mice injected with shIL22-transfected CTCL cells, and found no tumor invasion or metastasis in the inoculated mice, although the control mice showed multiple tumor invasions and metastases. These results, along with our previous data, demonstrated that miR-26 is a tumor suppressor that is associated with tumor invasion and the metastasis of advanced CTCL by regulating the IL-22–STAT3–CCL20 cascade. Therefore, a IL-22-targeting therapy could be a novel therapeutic strategy for advanced CTCL. |
|
言語 |
en |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 書誌情報 |
en : Cancer Science
巻 113,
号 4,
p. 1208-1219,
発行日 2022
|
| 収録物識別子 |
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|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
13479032 |
| 出版者 |
|
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出版者 |
John Wiley and Sons Inc |
| 関連情報 |
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関連タイプ |
isIdenticalTo |
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識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1111/cas.15296 |
| 権利情報 |
|
|
権利情報 |
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction
in any medium, provided the original work is properly cited and is not used for commercial purposes.© 2022 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. |
iA_2022_28.pdf (847.1 kB)
