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  1. 広島大学の刊行物
  2. Hiroshima Journal of Medical Sciences
  3. 60巻2号

Mel-18 Controls the Enrichment of Tumor-initiating Cells in SP Fraction in Mouse Breast Cancer

https://hiroshima.repo.nii.ac.jp/records/2013642
https://hiroshima.repo.nii.ac.jp/records/2013642
49274fa1-6784-4d2d-9572-10950804d74a
名前 / ファイル ライセンス アクション
HiroshimaJMedSci_60_25.pdf HiroshimaJMedSci_60_25.pdf (677.0 KB)
Item type デフォルトアイテムタイプ_(フル)(1)
公開日 2023-03-18
タイトル
タイトル Mel-18 Controls the Enrichment of Tumor-initiating Cells in SP Fraction in Mouse Breast Cancer
言語 en
作成者 Janakiraman, Harinarayanan

× Janakiraman, Harinarayanan

en Janakiraman, Harinarayanan

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Nobukiyo, Asako

× Nobukiyo, Asako

en Nobukiyo, Asako

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Inoue, Hiroko

× Inoue, Hiroko

en Inoue, Hiroko

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Kanno, Masamoto

× Kanno, Masamoto

en Kanno, Masamoto

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アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利情報
権利情報 (c) Hiroshima University Medical Press.
主題
主題Scheme Other
主題 Polycomb group
主題
主題Scheme Other
主題 Mel-18
主題
主題Scheme Other
主題 Side population
主題
主題Scheme Other
主題 Tumor-initiating cells
主題
主題Scheme Other
主題 NOD-SCID mice
主題
主題Scheme Other
主題 Abcg2
主題
主題Scheme NDC
主題 490
内容記述
内容記述 Side population (SP) cell analysis has been used to identify and isolate a minor population of cells with stem cell properties in normal tissues and in many cancers including breast cancer cells. However, the molecular mechanisms that operate in tumor-initiating cells (TICs) in SP fraction remain unclear. The Polycomb group genes, including Bmi1 and Mel-18, have been implicated in the maintenance of hematopoietic stem cells (HSCs) and suggested to be oncogenic and tumor suppressive, respectively, in breast cancer. In this study, we determined the critical role of Mel-18 in the enrichment mechanisms of TICs with the SP phenotype in a mouse breast cancer cell line, MMK3, that was established from a breast cancer developed spontaneously in Mel-18+/- mice. The Mel-18 protein expression level significantly correlates to the percentage of SP fraction in the mouse breast cancer cell line MMK3 series. The comparison between MMK3V3 (V3) cells containing one copy of the Mel-18 gene and MMK3S2 (S2) cells having twice the amount of Mel-18 expression clearly demonstrates the above relationship. Similar results obtained with the percentage of ALDH+ cells in V3 and S2 further confirmed the correlation between protein expression level of Mel-18 and the TICs. More importantly, transplantation of SP and non-SP cells of V3 and S2 cells into the NOD/SCID mice clearly showed that the heterozygous level of Mel-18 leads to the disappearance of enrichment of TICs into SP fraction in vivo. Stem cell pathway focused gene expression profiling of V3 and S2 cells revealed that the genes Abcg2, Aldh1a1 and Dhh were highly down-regulated in V3 compared to S2. These results indicate that the precise Mel-18 expression level controls TIC enrichment mechanisms through the regulation of channel molecule of Abcg2 and functional TIC marker of Aldh1a1. In conclusion, our findings revealed the significance of fine-tuning mechanisms for Mel-18 protein expression level in the maintenance of TIC into SP fractions in mouse breast cancer
言語 en
出版者
出版者 Hiroshima University Medical Press
言語
言語 eng
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 departmental bulletin paper
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 0018-2052
収録物識別子
収録物識別子タイプ NCID
収録物識別子 AA00664312
開始ページ
開始ページ 25
書誌情報 Hiroshima Journal of Medical Sciences
Hiroshima Journal of Medical Sciences

巻 60, 号 2, p. 25-35, 発行日 2011-06
旧ID 34991
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