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人γ干扰素对人骨肉瘤细胞生长的促进作用。

Enhancement of the growth of human osteosarcoma cells by human interferon-gamma.

作者信息

Tong L J, Yamaguchi N, Kita M, Imanishi J

机构信息

Department of Microbiology, Kyoto Prefectural University of Medicine, Japan.

出版信息

Cell Struct Funct. 1992 Oct;17(5):257-61. doi: 10.1247/csf.17.257.

DOI:10.1247/csf.17.257
PMID:1473155
Abstract

It is well known that interferons inhibit cell growth. However, we found that human interferon-gamma (HuIFN-gamma) enhanced the growth of human osteosarcoma cells, HOS-Y1 cells, in a dose-dependent manner. This enhancing effect was found only under the following conditions: when the cells were precultured for 2 or 3 days and then treated with HuIFN-gamma for 2, 3, or 4 days, and when the cells were seeded at a density of 1,000 or 2,000 cells/well. The degree of enhancement of cell growth was maximum when the cells were precultured at a density of 1,000 cells/well for 3 days and then treated with HuIFN-gamma for 2 days. The enhancing effect of HuIFN-gamma disappeared in the presence of anti-HuIFN-gamma antibody. In addition, it was found that the conditioned medium from HOS-Y1 cells enhanced the growth of HOS-Y1 cells, and that the conditioned medium from HOS-Y1 cells cultured with HuIFN-gamma enhanced the cell growth more than that from cells cultured without HuIFN-gamma. Epidermal growth factor (EGF), acidic fibroblast growth factor (aFGF), basic fibroblast growth factor (bFGF), and transforming growth factor-beta 1(TGF-beta 1) did not enhance the growth of HOS-Y1 cells. These results suggest that HuIFN-gamma enhanced the cell growth by augmenting the production of unknown growth factor(s) in HOS-Y1 cells via an autocrine mechanism.

摘要

众所周知,干扰素会抑制细胞生长。然而,我们发现人γ干扰素(HuIFN-γ)能以剂量依赖的方式促进人骨肉瘤细胞HOS-Y1细胞的生长。仅在以下条件下发现这种促进作用:当细胞预培养2或3天,然后用HuIFN-γ处理2、3或4天,以及当细胞以1000或2000个细胞/孔的密度接种时。当细胞以1000个细胞/孔的密度预培养3天,然后用HuIFN-γ处理2天时,细胞生长的促进程度最大。在抗HuIFN-γ抗体存在的情况下,HuIFN-γ的促进作用消失。此外,发现来自HOS-Y1细胞的条件培养基能促进HOS-Y1细胞的生长,并且与未用HuIFN-γ培养的细胞相比,用HuIFN-γ培养的HOS-Y1细胞的条件培养基对细胞生长的促进作用更大。表皮生长因子(EGF)、酸性成纤维细胞生长因子(aFGF)、碱性成纤维细胞生长因子(bFGF)和转化生长因子-β1(TGF-β1)均未促进HOS-Y1细胞的生长。这些结果表明,HuIFN-γ通过自分泌机制增加HOS-Y1细胞中未知生长因子的产生来促进细胞生长。

相似文献

1
Enhancement of the growth of human osteosarcoma cells by human interferon-gamma.人γ干扰素对人骨肉瘤细胞生长的促进作用。
Cell Struct Funct. 1992 Oct;17(5):257-61. doi: 10.1247/csf.17.257.
2
[Enhancement of cell growth by human interferons].
C R Seances Soc Biol Fil. 1990;184(2):187-92.
3
Effects of hyperthermia on the in vitro antiproliferative activities of HuIFN-alpha, HuIFN-beta, and rHuIFN-gamma employed separately and in combination.热疗对单独及联合使用的人α干扰素、人β干扰素和重组人γ干扰素体外抗增殖活性的影响。
J Biol Regul Homeost Agents. 1988 Jul-Sep;2(3):145-54.
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Liposomal transfection of human gamma-interferon gene into human glioma cells and adoptive immunotherapy using lymphokine-activated killer cells.将人γ-干扰素基因脂质体转染到人胶质瘤细胞中,并使用淋巴因子激活的杀伤细胞进行过继性免疫治疗。
J Neurosurg. 1994 Mar;80(3):510-4. doi: 10.3171/jns.1994.80.3.0510.
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Dipyridamole enhances an anti-proliferative effect of interferon in various types of human tumor cells.
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Comparative analysis of the influences of human gamma, alpha and beta interferons on human multipotential (CFU-GEMM), erythroid (BFU-E) and granulocyte-macrophage (CFU-GM) progenitor cells.人γ、α和β干扰素对人多能(CFU-GEMM)、红系(BFU-E)和粒-巨噬细胞(CFU-GM)祖细胞影响的比较分析。
J Immunol. 1983 Sep;131(3):1300-5.
7
Mouse monoclonal antibody with specificity for human interferon gamma.
Hybridoma. 1983;2(4):439-49. doi: 10.1089/hyb.1983.2.439.
8
Monoclonal antibodies neutralizing the antiviral and the antiproliferative activities of human interferon gamma.
Acta Virol. 1988 Jul;32(4):334-8.
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Human interferon-gamma enhances expression of ganglioside GM2 on human lung cancer cells and their susceptibility for antiganglioside GM2 monoclonal antibody-dependent cellular cytotoxicity.人干扰素-γ增强人肺癌细胞上神经节苷脂GM2的表达及其对抗神经节苷脂GM2单克隆抗体依赖性细胞毒性的敏感性。
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10
Gamma interferon induces colony-forming cells of the human monoblast cell line U937 to respond to inhibition by lactoferrin, transferrin, and acidic isoferritins.γ干扰素可诱导人单核细胞系U937的集落形成细胞对乳铁蛋白、转铁蛋白和酸性异铁蛋白的抑制作用产生反应。
Exp Hematol. 1986 Jan;14(1):35-43.

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