ID | 66566 |
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Author |
Katayama, Haruyoshi
Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Fujimura, Atsushi
Department of Cellular Physiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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Huang, Rongsheng
Department of Trauma Orthopedics, The Second Hospital of Dalian Medical University
Otani, Yusuke
Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Itano, Takuto
Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Fujiwara, Tomohiro
Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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Kunisada, Toshiyuki
Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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Nakata, Eiji
Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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Ozaki, Toshifumi
Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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Abstract | Malignant peripheral nerve sheath tumors (MPNSTs) are malignant tumors that are derived from Schwann cell lineage around peripheral nerves. As in many other cancer types, cancer stem cells (CSCs) have been identified in MPNSTs, and they are considered the cause of treatment resistance, recurrence, and metastasis. As an element defining the cancer stemness of MPNSTs, we previously reported a molecular mechanism by which exogenous adrenaline activates a core cancer stemness factor, YAP/TAZ, through β2 adrenoceptor (ADRB2). In this study, we found that MPNST cells express catecholamine synthases and that these enzymes are essential for maintaining cancer stemness, such as the ability to self-renew and maintain an undifferentiated state. Through gene knockdown and inhibition of these enzymes, we confirmed that catecholamines are indeed synthesized in MPNST cells. The results confirmed that catecholamine synthase knockdown in MPNST cells reduces the activity of YAP/TAZ. These data suggest that a mechanism of YAP/TAZ activation by de novo synthesized adrenaline, as well as exogenous adrenaline, may exist in the maintenance of cancer stemness of MPNST cells. This mechanism not only helps to understand the pathology of MPNST, but could also contribute to the development of therapeutic strategies for MPNST.
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Keywords | benserazide
cancer stem cell
catecholamine synthase
malignant peripheral nerve sheath tumor
Schwann cell
vesicular monoamine transporter
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Published Date | 2024-01-26
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Publication Title |
Cancer Science
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Volume | volume115
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Issue | issue3
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Publisher | Wiley
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Start Page | 871
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End Page | 882
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ISSN | 1347-9032
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NCID | AA11808050
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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 | © 2024 The Authors.
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File Version | publisher
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PubMed ID | |
DOI | |
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Related Url | isVersionOf https://doi.org/10.1111/cas.16077
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License | https://creativecommons.org/licenses/by-nc/4.0/
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Citation | Katayama H, Fujimura A, Huang R, et al. Role of catecholamine synthases in the maintenance of cancer stem-like cells in malignant peripheral nerve sheath tumors. Cancer Sci. 2024; 115: 871-1. doi:10.1111/cas.16077
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Funder Name |
Ministry of Education, Culture, Sports, Science and Technology
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助成番号 | JP23771889
JP23773811
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