| Item type |
文献 / Documents(1) |
| 公開日 |
2023-08-31 |
| アクセス権 |
|
|
アクセス権 |
open access |
| 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 |
| 出版社版DOI |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1186/s13046-022-02304-6 |
|
|
言語 |
ja |
|
|
関連名称 |
10.1186/s13046-022-02304-6 |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
Inhibition of the mitochondrial protein Opa1 curtails breast cancer growth |
|
言語 |
en |
| 著者 |
Zamberlan, Margherita
Boeckx, Amandine
Muller, Florian
Vinelli, Federica
Ek, Olivier
Vianello, Caterina
Coart, Emeline
柴田, 桂太朗
Christian, Aurélie
Grespi, Francesca
Giacomello, Marta
Struman, Ingrid
Scorrano, Luca
Herkenne, Stéphanie
|
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Background: Mitochondrial fusion and fission proteins have been nominated as druggable targets in cancer. Whether their inhibition is efficacious in triple negative breast cancer (TNBC) that almost invariably develops chemoresistance is unknown.
Methods: We used a combination of bioinformatics analyses of cancer genomic databases, genetic and pharmacological Optic Atrophy 1 (OPA1) inhibition, mitochondrial function and morphology measurements, micro-RNA (miRNA) profiling and formal epistatic analyses to address the role of OPA1 in TNBC proliferation, migration, and invasion in vitro and in vivo.
Results: We identified a signature of OPA1 upregulation in breast cancer that correlates with worse prognosis. Accordingly, OPA1 inhibition could reduce breast cancer cells proliferation, migration, and invasion in vitro and in vivo. Mechanistically, while OPA1 silencing did not reduce mitochondrial respiration, it increased levels of miRNAs of the 148/152 family known to inhibit tumor growth and invasiveness. Indeed, these miRNAs were epistatic to OPA1 in the regulation of TNBC cells growth and invasiveness.
Conclusions: Our data show that targeted inhibition of the mitochondrial fusion protein OPA1 curtails TNBC growth and nominate OPA1 as a druggable target in TNBC. |
|
言語 |
en |
| 書誌情報 |
en : Journal of Experimental & Clinical Cancer Research
巻 41,
p. 95,
発行日 2022-03-12
|
| 収録物ID |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
17569966 |
| 出版者 |
|
|
出版者 |
Springer Nature |
|
言語 |
en |
| 出版者 |
|
|
出版者 |
BioMed Central |
|
言語 |
en |
| 権利情報 |
|
|
言語 |
en |
|
権利情報 |
© The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
| EID |
|
|
識別子 |
400056 |
|
識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
jeccr_41_95.pdf (8.55 MB)
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