ID | 65499 |
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Author |
Okada, Nobuhiro
Graduate School of Interdisciplinary Science & Engineering in Health Systems, Okayama University
Kaken ID
researchmap
Ueki, Chihiro
Graduate School of Interdisciplinary Science & Engineering in Health Systems, Okayama University
Shimazaki, Masahiro
Laboratory for Malignancy Control Research, Medical Innovation Center, Kyoto University
Tsujimoto, Goki
Graduate School of Interdisciplinary Science & Engineering in Health Systems, Okayama University
Kohno, Susumu
Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University
Muranaka, Hayato
Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University
Yoshikawa, Kiyotsugu
Faculty of Pharmaceutical Sciences, Doshisha Women’s College of Liberal Arts
Takahashi, Chiaki
Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University
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Abstract | Two splicing variants exist in NFYA that exhibit high expression in many human tumour types. The balance in their expression correlates with prognosis in breast cancer, but functional differences remain unclear. Here, we demonstrate that NFYAv1, a long-form variant, upregulates the transcription of essential lipogenic enzymes ACACA and FASN to enhance the malignant behavior of triple-negative breast cancer (TNBC). Loss of the NFYAv1-lipogenesis axis strongly suppresses malignant behavior in vitro and in vivo, indicating that the NFYAv1-lipogenesis axis is essential for TNBC malignant behavior and that the axis might be a potential therapeutic target for TNBC. Furthermore, mice deficient in lipogenic enzymes, such as Acly, Acaca, and Fasn, exhibit embryonic lethality; however, Nfyav1-deficient mice exhibited no apparent developmental abnormalities. Our results indicate that the NFYAv1-lipogenesis axis has tumour-promoting effects and that NFYAv1 may be a safe therapeutic target for TNBC.
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Note | The version of record of this article, first published in Communications Biology, is available online at Publisher’s website: http://dx.doi.org/10.1038/s42003-023-04987-9
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Published Date | 2023-06-02
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Publication Title |
Communications Biology
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Volume | volume6
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Issue | issue1
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Publisher | nature portfolio
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Start Page | 596
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ISSN | 2399-3642
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Content Type |
Journal Article
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language |
English
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OAI-PMH Set |
岡山大学
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Copyright Holders | © The Author(s) 2023
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File Version | publisher
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PubMed ID | |
DOI | |
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Related Url | isVersionOf https://doi.org/10.1038/s42003-023-04987-9
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License | http://creativecommons.org/licenses/by/4.0/
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Citation | Okada, N., Ueki, C., Shimazaki, M. et al. NFYA promotes malignant behavior of triple-negative breast cancer in mice through the regulation of lipid metabolism. Commun Biol 6, 596 (2023). https://doi.org/10.1038/s42003-023-04987-9
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Funder Name |
Japan Society for the Promotion of Science
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助成番号 | JP16H06276
JP22K07152
JP19K07640
JP15K18407
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