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Cleavage of growth differentiation factor 15 (GDF15) by membrane type 1-matrix metalloproteinase abrogates GDF15-mediated suppression of tumor cell growth
https://doi.org/10.24517/00027536
https://doi.org/10.24517/00027536251473f1-ae22-43f3-ae14-38f7cbda59f5
名前 / ファイル | ライセンス | アクション |
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CA-PR-SATO-H-1330.pdf (264.0 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-05 | |||||
タイトル | ||||||
タイトル | Cleavage of growth differentiation factor 15 (GDF15) by membrane type 1-matrix metalloproteinase abrogates GDF15-mediated suppression of tumor cell growth | |||||
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 | journal article | |||||
ID登録 | ||||||
ID登録 | 10.24517/00027536 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Abd El-Aziz, Shaban H.
× Abd El-Aziz, Shaban H.× Endo, Yoshio× Miyamaori, Hisashi× Takino, Takashi× Sato, Hiroshi |
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著者別表示 |
遠藤, 良夫
× 遠藤, 良夫× 宮森, 久志× 滝野, 隆久× 佐藤, 博 |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学がん研究所がん病態制御 | |||||
書誌情報 |
Cancer Science 巻 98, 号 9, p. 1330-1335, 発行日 2007-09-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1347-9032 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA11808050 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1111/j.1349-7006.2007.00547.x | |||||
出版者 | ||||||
出版者 | Japanese Cancer Association / Blackwell Publishing | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Growth differentiation factor 15 (GDF15), a transforming growth factor (TGF)-β superfamily member, has been cloned from a placenta cDNA library as a gene product that has promoted activation of pro-matrix metalloproteinase (MMP)2 mediated by membrane type (MT)1-MMP. Expression of MT1-MMP in HEK293T cells caused cleavage of the GDF15 mature form at N252 -M253 to produce a 6-kDa C -terminal fragment. Treatment of MCF7 cells with GDF15 induced activation of p53 and enhanced expression of p21, which was abrogated by MT1-MMP expression. GDF15 mRNA synthesis was also shown to be induced by treatment of cells with GDF15. Treatment of MCF7 cells with GDF15 caused suppression of cell proliferation. However, proliferation of MCF7 cells transfected with the MT1-MMP gene was not affected by GDF15 treatment, but was suppressed in the presence of the MMP inhibitor BB94. HT1080 cells transfected with the GDF15 gene, which endogenously express MT1-MMP, synthesize a high-level GDF15 precursor form and a low-level mature form, and treatment of cells with BB94 enhanced production of the GDF15 mature form. Consistent with GDF15 production, HT1080 cells transfected with the GDF15 gene proliferated almost equally with control cells, and addition of BB94 effectively suppressed growth of HT1080 cells transfected with the GDF15 gene concomitant with the accumulation of the GDF15 mature form, but not control cells. These results suggest that MT1-MMP contributes to tumor cell proliferation through the cleavage of GDF15, which down-regulates cell proliferation by inducing activation of p53 and p21 synthesis. © 2007 Japanese Cancer Association. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |