Role of Tissue Inhibitor of Metalloproteinases-2(TIMP-2) in Regulation of Pro-Gelatinase A Activation Catalyzed by Membrane-Type Matrix Metalloproteinase-1(MT1-MMP) in Human Cancer Cells.
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概要
- 論文の詳細を見る
To clarify the regulatory mechanism of pro-gelatinase A (proGelA) activation at a cellular level, expression of gelatinase A (GelA), three MT-MMPs, and TIMP-2 was examined with 11 human cancer cell lines cultured in the presence and absence of stimulants. MT1-MMP mRNA was expressed in 8 cell lines, while MT2-MMP and MT3-MMP mRNAs were expressed in fewer cell lines. The cells with high proGelA activation strongly expressed MT1-MMP mRNA but not MT2-MMP and MT3-MMP mRNAs, suggesting that MT1-MMP was responsible for the proGelA activation in the cancer cells. Treatments with concanavalin A (Con A) and a phorbor ester (TPA) enhanced the MT1-MMP expression, but only Con A stimulated the proGelA activation in many cell lines. In HT1080 fibrosarcoma cells, however, TPA also stimulated the activation. The level of TIMP-2 secreted into culture medium inversely correlated with proGelA activation. For example, 2 squamous cell carcinoma lines (HSC-3 and HSC-4) and 3 HT1080 clones, which efficiently activated proGelA, secreted little TIMP-2 into medium, whereas other cell lines and other HT1080 clones, which hardly activated proGelA, secreted TIMP-2 at high levels. When HSC-3 cells were incubated with TIMP-2 protein or transfected with TIMP-2 cDNA, the proGelA activation was strongly inhibited. These results indicated that extracellular TIMP-2 was an important negative regulator of proGelA activation. However, the level of extracellular TIMP-2 was not consistent with that of TIMP-2 mRNA in some cell lines. Other experimental results suggested that TIMP-2 might be rapidly metabolized after binding to MT1-MMP, and Con A treatment might stabilize the complex of TIMP-2 and MT1-MMP on cell membranes.
- 社団法人 日本生化学会の論文
著者
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Miki Keizaburo
Institutc For Biomedical Science Terumo R&d Center.
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Yasumitsu Hidetaro
Division Of Cell Biology Kihara Institute For Biological Research Yokohama City University
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Miyazaki Kaoru
Division Of Cell Biology Kihara Insitutc For Biomedical Rescarch Yokohama City University.
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Nishihashi Ai
Division Of Cell Biology Kihara Insitutc For Biomedical Rescarch Yokohama City University.
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Sato Hiroshi
Department Of Anatomy And Developmental Neurobiology Institute Of Health Biosciences The University
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Mizushima Hiroto
Division Of Cell Biology Kihara Insitutc For Biomedical Rescarch Yokohama City University.
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Higashi Shouichi
Division Of Cell Biology Kihara Institute For Biological Research Yokohama City University
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Seiki Motoharu
Department Of Cancer Cell Research Institute Of Medical Science The University Of Tokyo.
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Shofuda Ken-ichi
Division of Cell Biology,Kihara Insitutc for Biomedical Rescarch Yokohama City University.
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Moriyama Kayano
Division of Cell Biology, Kihara Institute for Biological Research, Yokohama City University
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