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タイトル: SLAM family member 8 is expressed in and enhances the growth of anaplastic large cell lymphoma
著者: Sugimoto, Akihiko
Kataoka, Tatsuki R.
Ito, Hiroaki
Kitamura, Kyohei
Saito, Narumi
Hirata, Masahiro
Ueshima, Chiyuki
Takei, Yusuke
Moriyoshi, Koki
Otsuka, Yasuyuki
Nishikori, Momoko  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0003-4171-2162 (unconfirmed)
Takaori-Kondo, Akifumi
Haga, Hironori  kyouindb  KAKEN_id
著者名の別形: 片岡, 竜貴
錦織, 桃子
髙折, 晃史
羽賀, 博典
発行日: 13-Feb-2020
出版者: NLM (Medline)
誌名: Scientific reports
巻: 10
論文番号: 2505
抄録: Signaling lymphocytic activation molecule family member 8 (SLAMF8)
B-lymphocyte activator macrophage expressed/CD353 is a member of the CD2 family. SLAMF8 suppresses macrophage function but enhances the growth of neoplastic mast cells via SHP-2. In this study, we found that some anaplastic large cell lymphoma (ALCL) samples were immunohistochemically positive for SLAMF8. However, we found no significant differences between SLAMF8-positive and SLAMF8-negative ALCL samples with respect to age, gender, site, or prognosis. We also identified SLAMF8 expression in ALCL cell lines, Karpas299, and SU-DHL-1. SLAMF8 knockdown decreased the activation of SHP-2 and the growth of these cell lines, and increased the apoptosis of these cell lines. In addition, we observed the interaction between SLAMF8 and SHP-2 in these cell lines using the DuoLink in situ kit. Taken together, these results suggest that SLAMF8 may enhance the growth of ALCL via SHP-2 interaction.
著作権等: 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.
URI: http://hdl.handle.net/2433/255846
DOI(出版社版): 10.1038/s41598-020-59530-1
PubMed ID: 32054954
出現コレクション:学術雑誌掲載論文等

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