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[通过培养模型研究肿瘤细胞侵袭机制——宿主介质对侵袭性的调节]

[Mechanism of tumor cell invasion studied by a culture model--modification of invasiveness by host mediators].

作者信息

Mukai M, Shinkai K, Yoshioka K, Imamura F, Akedo H

机构信息

Department of Tumor Biochemistry, Research Institute Center for Adult Diseases, Osaka, Japan.

出版信息

Hum Cell. 1993 Sep;6(3):194-8.

PMID:8297816
Abstract

A culture model for invasion of rat mesothelial cell layer by rat ascites hepatoma cells has been developed. By using this quantitative model, we have recently found that the invasiveness of tumor cells is not only genetically determined but is greatly influenced by their interactions with host cells and host mediators. The preculture with macrophages was found to enhance both the in vitro and in vivo invasive potentials of the tumor cells. This potentiation appears to be mediated partly by oxygen radicals generated by the cocultured macrophages. The in vitro invasive capacity was also augmented by pretreating the tumor cells with TGF-beta, or with activated platelets. In the in vitro invasion assay system, tumor cells did not invade against cultured mesothelial cell monolayers without fetal calf serum. Serum could be completely substituted by oleoyl-lysophosphatidic acid (LPA) or bacterial phospholipase D (PLD), suggesting a possible participation of particular signaling cascade, PLD-LPA(PA) system, in the invasion of certain tumor cells.

摘要

已建立大鼠腹水肝癌细胞侵袭大鼠间皮细胞层的培养模型。通过使用这个定量模型,我们最近发现肿瘤细胞的侵袭性不仅由基因决定,还受到它们与宿主细胞和宿主介质相互作用的极大影响。发现与巨噬细胞预培养可增强肿瘤细胞的体外和体内侵袭潜能。这种增强作用似乎部分由共培养的巨噬细胞产生的氧自由基介导。用转化生长因子-β(TGF-β)或活化血小板预处理肿瘤细胞也可增强其体外侵袭能力。在体外侵袭试验系统中,没有胎牛血清时肿瘤细胞不会侵袭培养的间皮细胞单层。血清可被油酰溶血磷脂酸(LPA)或细菌磷脂酶D(PLD)完全替代,这表明特定信号级联反应,即PLD-LPA(PA)系统,可能参与某些肿瘤细胞的侵袭过程。

相似文献

1
[Mechanism of tumor cell invasion studied by a culture model--modification of invasiveness by host mediators].[通过培养模型研究肿瘤细胞侵袭机制——宿主介质对侵袭性的调节]
Hum Cell. 1993 Sep;6(3):194-8.
2
Potentiation and inhibition of tumor cell invasion by host cells and mediators.宿主细胞和介质对肿瘤细胞侵袭的增强和抑制作用。
Invasion Metastasis. 1989;9(2):134-48.
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Induction of in vitro tumor cell invasion of cellular monolayers by lysophosphatidic acid or phospholipase D.溶血磷脂酸或磷脂酶D诱导细胞单层的体外肿瘤细胞侵袭
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Macrophage potentiation of invasive capacity of rat ascites hepatoma cells.
Cancer Res. 1987 Apr 15;47(8):2167-71.
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[Establishment of an experimental model for tumor cell invasion and potentiation and inhibition of the invasive capacity].[肿瘤细胞侵袭及侵袭能力增强与抑制的实验模型的建立]
Gan To Kagaku Ryoho. 1987 Jun;14(6 Pt 2):2048-55.
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Interaction of rat ascites hepatoma cells with cultured mesothelial cell layers: a model for tumor invasion.大鼠腹水肝癌细胞与培养的间皮细胞层的相互作用:肿瘤侵袭模型
Cancer Res. 1986 May;46(5):2416-22.
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Microglia-derived TGF-beta as an important regulator of glioblastoma invasion--an inhibition of TGF-beta-dependent effects by shRNA against human TGF-beta type II receptor.小胶质细胞衍生的转化生长因子-β作为胶质母细胞瘤侵袭的重要调节因子——通过针对人转化生长因子-β II型受体的短发夹RNA抑制转化生长因子-β依赖性效应
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Overexpression of small GTP-binding protein RhoA promotes invasion of tumor cells.小GTP结合蛋白RhoA的过表达促进肿瘤细胞的侵袭。
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Potentiation of invasive capacity of rat ascites hepatoma cells by adriamycin.
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RhoC is essential for TGF-beta1-induced invasive capacity of rat ascites hepatoma cells.RhoC对于转化生长因子β1诱导的大鼠腹水肝癌细胞侵袭能力至关重要。
Biochem Biophys Res Commun. 2006 Jul 21;346(1):74-82. doi: 10.1016/j.bbrc.2006.05.068. Epub 2006 May 19.

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