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DCフィールド | 値 | 言語 |
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dc.contributor.author | Zhang, Shuang | en |
dc.contributor.author | Harada, Masayuki | en |
dc.contributor.author | Kimura, Takeshi | en |
dc.contributor.author | Ashida, Noboru | en |
dc.contributor.alternative | 張, 爽 | ja |
dc.contributor.alternative | 原田, 雅之 | ja |
dc.contributor.alternative | 木村, 剛 | ja |
dc.contributor.alternative | 芦田, 昇 | ja |
dc.date.accessioned | 2024-03-01T01:26:17Z | - |
dc.date.available | 2024-03-01T01:26:17Z | - |
dc.date.issued | 2022-09-17 | - |
dc.identifier.uri | http://hdl.handle.net/2433/287142 | - |
dc.description.abstract | Cancer-associated fibroblasts (CAFs) are a major component of the tumor microenvironment and play critical roles in tumorigenesis. CAFs consists of multiple subpopulations, which have diverse functions. The detailed mechanism, including the role of NF-κB, a critical transcription factor for inflammation and cell survival, in CAFs has not been adequately explored. In this study, we examined the roles of IKKβ, a key kinase for NF-κB activation, in activated CAFs by using mice (KO mice) with deletion of IKKβ in activated fibroblasts (aFbs). We found that melanoma cells implanted in KO mice showed significantly more growth than those implanted in control mice. To exclude the effects of deletion of IKKβ in cells other than aFbs, we implanted a mixture of melanoma cells and IKKβ-deleted aFbs in wild-type mice and observed that the mixture showed greater growth than a mixture of melanoma cells and normal aFbs. In exploring the mechanisms, we found that conditioned medium from IKKβ-deleted aFbs promotes the proliferation of melanoma cells, and the expression of growth arrest-specific 6 (GAS6) and hepatocyte growth factor (HGF), which are major tumor-promoting factors, was upregulated in IKKβ-deleted aFbs. These results indicated the tumor-suppressing function of IKKβ in activated CAFs. | en |
dc.language.iso | eng | - |
dc.publisher | Elsevier BV | en |
dc.rights | © 2022 The Authors. Published by Elsevier Inc. | en |
dc.rights | This is an open access article under the CC BY-NC-ND license. | en |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | - |
dc.subject | Cancer-associated Fibroblast | en |
dc.subject | NF-κB | en |
dc.subject | IKKβ | en |
dc.title | Deletion of IKKβ in activated fibroblasts promotes tumor progression in melanoma | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | Biochemical and Biophysical Research Communications | en |
dc.identifier.volume | 621 | - |
dc.identifier.spage | 46 | - |
dc.identifier.epage | 52 | - |
dc.relation.doi | 10.1016/j.bbrc.2022.07.004 | - |
dc.textversion | publisher | - |
dc.identifier.pmid | 35810590 | - |
dcterms.accessRights | open access | - |
datacite.awardNumber | 25461497 | - |
datacite.awardNumber | 16H05297 | - |
datacite.awardNumber | 18K08068 | - |
datacite.awardNumber | 21K08103 | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25461497/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16H05297/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18K08068/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21K08103/ | - |
dc.identifier.pissn | 0006-291X | - |
dc.identifier.eissn | 1090-2104 | - |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.awardTitle | 新規の線維化・強皮症モデルマウスを用いた炎症-自己免疫-線維化相互関連の解明 | ja |
jpcoar.awardTitle | Neoatherosclerosisと退行性血管病変の本態解明と治療法開発 | ja |
jpcoar.awardTitle | 新規血管石灰化マウスを用いた大動脈弁狭窄症のメカニズム解析 | ja |
jpcoar.awardTitle | 非心筋細胞における炎症シグナルをターゲットとした心筋炎新規治療法の開発 | ja |
出現コレクション: | 学術雑誌掲載論文等 |
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