{"created":"2023-07-25T10:25:35.113706+00:00","id":5996,"links":{},"metadata":{"_buckets":{"deposit":"ef94b3b3-37d1-42a5-89c9-d3b6ace2eb12"},"_deposit":{"created_by":3,"id":"5996","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"5996"},"status":"published"},"_oai":{"id":"oai:air.repo.nii.ac.jp:00005996","sets":["611:939:940"]},"author_link":["18041","18042","18037","18038","18040","18039"],"item_10001_biblio_info_7":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2012","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"7","bibliographicVolumeNumber":"7","bibliographic_titles":[{"bibliographic_title":"PLOS ONE"}]}]},"item_10001_description_5":{"attribute_name":"内容記述(抄録)","attribute_value_mlt":[{"subitem_description":"Uterine leiomyosarcoma is an aggressive tumor typically found at advanced stages due to difficulties with early diagnosis. Because uterine leiomyosarcoma is resistant to conventional radiation and chemotherapy, the development of more potent medical therapeutics is anticipated. Using quantitative real-time RT-PCR and immunostaining, we found the expression of brain-derived neurotrophic factor (BDNF) and neurotropin-4/5, together with their receptor, tyrosine kinase B (TrkB), in different uterine sarcoma cell lines and primary tumor samples from uterine leiomyosarcoma patients. We noted that levels of BDNF were more abundant than those of neurotropin-4/5. Moreover, the expression of TrkB and its ligands was elevated in a multidrug-resistant cell line and samples obtained from patients with leiomyosarcoma. In cultured uterine sarcoma cells, inhibition of endogenous TrkB signaling by treatment with either the soluble TrkB ectodomain or the Trk receptor inhibitor, K252a, suppressed cell proliferation and increased apoptosis based on cell viability and proliferation, in situ terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick end-labeling and caspase-3/7 assays, whereas an inactive plasma membrane nonpermeable K252b was ineffective. Correspondingly, treatment with exogenous BDNF increased cell proliferation. In in vivo studies in athymic nude mice bearing multidrug-resistant uterine sarcoma cell tumors, we demonstrate suppression of tumor growth by treatment with K252a, but not K252b, as reflected by decreased cell proliferation and increased levels of apoptosis and caspase-3/7 activities without obvious side effects. Our findings indicated that endogenous signaling of the TrkB pathway contributed to uterine sarcoma cell growth, and inhibition of TrkB signaling in these tumors could provide a novel medical therapy for patients with uterine sarcomas.","subitem_description_type":"Other"}]},"item_10001_publisher_8":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Public Library of Science"}]},"item_10001_relation_14":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"10.1371/journal.pone.0041049","subitem_relation_type_select":"DOI"}}]},"item_10001_relation_25":{"attribute_name":"関連リンク","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"http://dx.doi.org/10.1371/journal.pone.0041049"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://dx.doi.org/10.1371/journal.pone.0041049","subitem_relation_type_select":"DOI"}}]},"item_10001_rights_15":{"attribute_name":"著作権等","attribute_value_mlt":[{"subitem_rights":"© 2012 Makino et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited."}]},"item_10001_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"1932-6203","subitem_source_identifier_type":"ISSN"}]},"item_10001_version_type_20":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Makino, Kenichi"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Kawamura, Kazuhiro"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Sato, Wataru"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Kawamura, Nanami"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Fujimoto, Toshio"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Terada, Yukihiro"}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2023-02-25"}],"displaytype":"detail","filename":"iA_2022_115.pdf","filesize":[{"value":"612.6 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"iA_2022_115.pdf","url":"https://air.repo.nii.ac.jp/record/5996/files/iA_2022_115.pdf"},"version_id":"623c0e75-3c8c-4dc9-8eb4-e9a94954f6f3"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"Inhibition of Uterine Sarcoma Cell Growth through Suppression of Endogenous Tyrosine Kinase B Signaling","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Inhibition of Uterine Sarcoma Cell Growth through Suppression of Endogenous Tyrosine Kinase B Signaling"}]},"item_type_id":"10001","owner":"3","path":["940"],"pubdate":{"attribute_name":"公開日","attribute_value":"2023-02-25"},"publish_date":"2023-02-25","publish_status":"0","recid":"5996","relation_version_is_last":true,"title":["Inhibition of Uterine Sarcoma Cell Growth through Suppression of Endogenous Tyrosine Kinase B Signaling"],"weko_creator_id":"3","weko_shared_id":-1},"updated":"2023-07-25T10:38:47.276727+00:00"}