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  1. 教員研究業績
  2. 臨床薬剤学研究室
  3. 原著論文

Regulation of lysyl oxidase expression in THP‐1 cell‐derived M2‐like macrophages

https://gifu-pu.repo.nii.ac.jp/records/14269
https://gifu-pu.repo.nii.ac.jp/records/14269
5b2a0c9b-bdfe-4606-8bb7-d26c79915031
Item type 研究室原著論文(1)
公開日 2021-03-04
タイトル
タイトル Regulation of lysyl oxidase expression in THP‐1 cell‐derived M2‐like macrophages
タイトル
タイトル Regulation of lysyl oxidase expression in THP‐1 cell‐derived M2‐like macrophages
言語 en
言語
言語 eng
キーワード
主題Scheme Other
主題 FOXO1
キーワード
主題Scheme Other
主題 HIF1α
キーワード
主題Scheme Other
主題 lysyl oxidase
キーワード
主題Scheme Other
主題 macrophage
キーワード
主題Scheme Other
主題 STAT3
キーワード
主題Scheme Other
主題 tumor microenvironment
キーワード
言語 en
主題Scheme Other
主題 FOXO1
キーワード
言語 en
主題Scheme Other
主題 HIF1α
キーワード
言語 en
主題Scheme Other
主題 lysyl oxidase
キーワード
言語 en
主題Scheme Other
主題 macrophage
キーワード
言語 en
主題Scheme Other
主題 STAT3
キーワード
言語 en
主題Scheme Other
主題 tumor microenvironment
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
抄録
値 Lysyl oxidase (LOX) is a copper‐containing enzyme and its overexpression in tumor tissues promote tumor metastasis through the crosslinking of extracellular matrix. Our previous report demonstrated that LOX expression is significantly increased in human leukemic THP‐1 cell‐derived M2‐like macrophages, and histone modification plays a key role in its induction. However, the rigorous mechanism of LOX regulation remains unclear. In this study, we investigated the role of functional transcription factors, hypoxia‐inducible factor 1α (HIF1α), sig- nal transducer and activator of transcription 3 (STAT3) and forkhead box O1 (FOXO1) in LOX regulation in M2‐like macrophages. HIF1α expression was significantly increased in M2‐like macrophages, and HIF1α inhibitor, TX402, suppressed LOX induction. The significant STAT3 activation was also observed in M2‐like macrophages. Additionally, LOX induction was canceled in the presence of STAT3 inhibitor, S3I‐201, suggesting that HIF1α and STAT3 pathways play a critical role in LOX induction. On the other hand, our ChIP results clearly indicated that the enrichment of FOXO1 within the lox promoter region was dramatically decreased in M2‐like macrophages. In this context, knockdown of FOXO1 further enhanced LOX induction. LOX induction and HIF1α binding to the lox promoter region were suppressed in FOXO1‐overexpressed cells, sug- gesting that the FOXO1 binding to the lox promoter region counteracted HIF1α binding to that region. Overall, the present data suggested that both of HIF1α and STAT3 were required for LOX induction in M2‐like macrophages, and loss of FOXO1 within the lox promoter region facilitated HIF1α binding to that region which promoted LOX induction.
書誌情報 Journal of Cellular Biochemistry
en : Journal of Cellular Biochemistry

発行日 2021
DOI
値 10.1002/jcb.29911
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