{"created":"2024-10-25T10:10:42.430945+00:00","id":2003312,"links":{},"metadata":{"_buckets":{"deposit":"f742d443-a372-43a3-8e61-bb11f31f3d94"},"_deposit":{"created_by":7,"id":"2003312","owners":[7],"pid":{"revision_id":0,"type":"depid","value":"2003312"},"status":"published"},"_oai":{"id":"oai:tokushima-u.repo.nii.ac.jp:02003312","sets":["1713853213384:1713853296295:1716267876683:1716268551628"]},"author_link":["1568","1546","1557","519","711"],"item_10001_alternative_title_1":{"attribute_name":"タイトル別表記","attribute_value_mlt":[{"subitem_alternative_title":"ガレクチン-3は、前立腺癌におけるアンドロゲン受容体シグナル伝達の調節を介して腫瘍進展および抗アンドロゲン剤耐性に関与している","subitem_alternative_title_language":"ja"},{"subitem_alternative_title":"Galectin-3 in Prostate Cancer","subitem_alternative_title_language":"en"}]},"item_10001_biblio_info_7":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2017-01","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"1","bibliographicPageEnd":"134","bibliographicPageStart":"125","bibliographicVolumeNumber":"37","bibliographic_titles":[{"bibliographic_title":"ANTICANCER RESEARCH","bibliographic_titleLang":"en"}]}]},"item_10001_description_5":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Background: Castration-resistant prostate cancer (CRPC)-related deaths are increasing worldwide. Therefore, clarification of the mechanisms of hormone-related tumor progression and resistance to anti-androgen drugs is useful in order to develop strategies for appropriate treatment of CRPC. Galectin-3 has been shown to be correlated with tumor progression in a variety of cancer types through the regulation of tumor proliferation, angiogenesis, and apoptosis. Materials and Methods: We examined tumor cell invasion and migration using the xCELLigence system. Control LNCaP and galectin- 3-expressing LNCaP (LNCaP-Gal-3) cells were cultured with androgen-depleted medium with 5% charcoal-stripped serum. Cells were treated for 24 h with or without dihydrotestosterone alone or combined with MDV3100 and bicalutamide; gene profile was then analyzed by microarray analysis and mRNA expression was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). We evaluated tumor growth using spheroids and xenograft tumor growth in a mouse model. Results: In vitro, LNCaP-Gal-3 cells promoted both cell migration and invasion in an androgen-independent manner compared to control LNCaP cells. Galectin-3 also enhanced anchorage-independent growth and xenograft tumor growth even after castration. Importantly, galectin-3 greatly enhanced transcriptional activity of the androgen receptor (AR), especially on treatment with dihydrotestosterone. In microarray and qRT-PCR analyses, galectin-3 increased the expression of several AR-target genes, such as kallikreinrelated peptidase 3 (KLK3), and transmembrane protease, serine 2 (TMPRSS2). These AR-target genes were not fully suppressed by anti-androgen drugs such as bicalutamide or MDV3100. Galectin-3 significantly inhibited the effect induced by anti-androgen drugs MDV3100 and bicalutamide, suggesting that galectin-3 may be involved in resistance to anti-androgen drug through enhancement of transcriptional activity of AR and expression of AR-related genes. Conclusion: These results suggest that galectin-3 is a potential target molecule for future treatment of anti-androgen drug-resistant prostate cancer.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_10001_publisher_8":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"The International Institute of Anticancer Research","subitem_publisher_language":"en"}]},"item_10001_source_id_9":{"attribute_name":"収録物ID","attribute_value_mlt":[{"subitem_source_identifier":"02507005","subitem_source_identifier_type":"ISSN"},{"subitem_source_identifier":"17917530","subitem_source_identifier_type":"ISSN"},{"subitem_source_identifier":"AA10625860","subitem_source_identifier_type":"NCID"},{"subitem_source_identifier":"AA12440673","subitem_source_identifier_type":"NCID"}]},"item_10001_version_type_20":{"attribute_name":"出版タイプ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_be7fb7dd8ff6fe43","subitem_version_type":"NA"}]},"item_1714461018643":{"attribute_name":"報告番号","attribute_value_mlt":[{"subitem_dissertationnumber":"甲第3011号"}]},"item_1714461102074":{"attribute_name":"学位名","attribute_value_mlt":[{"subitem_degreename":"博士（医学）","subitem_degreename_language":"ja"}]},"item_1714461118377":{"attribute_name":"学位授与年月日","attribute_value_mlt":[{"subitem_dategranted":"2017-02-23"}]},"item_1714461137393":{"attribute_name":"学位授与機関","attribute_value_mlt":[{"subitem_degreegrantor":[{"subitem_degreegrantor_language":"ja","subitem_degreegrantor_name":"徳島大学"}]}]},"item_1715043197608":{"attribute_name":"アクセス権","attribute_value_mlt":[{"subitem_access_right":"open access"}]},"item_1718868208704":{"attribute_name":"備考","attribute_value_mlt":[{"subitem_textarea_language":"ja","subitem_textarea_value":"内容要旨・審査要旨・論文本文の公開：\n内容要旨・審査要旨：LID201704261001.pdf\n論文本文：k3011_fulltext.pdf\n本論文は, 著者TSOGT-OCHIR DONDOOの学位論文として提出され, 学位審査・授与の対象となっている。\n公開に関する許諾確認は著者・編集事務局間のメールによる。\n学位授与者所属 : 徳島大学大学院医科学教育部（医学専攻）"}]},"item_1718868303842":{"attribute_name":"学位記番号","attribute_value_mlt":[{"subitem_text_language":"ja","subitem_text_value":"甲医第1315号"}]},"item_1722929371688":{"attribute_name":"出版社版DOI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_language":"ja","subitem_relation_name_text":"10.21873/anticanres.11297"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://doi.org/10.21873/anticanres.11297","subitem_relation_type_select":"DOI"}}]},"item_1723180141928":{"attribute_name":"EID","attribute_value_mlt":[{"subitem_identifier_type":"URI","subitem_identifier_uri":"343696"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"ドンドオ, ツォクトーオチル","creatorNameLang":"ja"},{"creatorName":"ドンドオ, ツォクトーオチル","creatorNameLang":"ja-Kana"},{"creatorName":"Dondoo, 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