GROWTH-CONTROL AND GENE-EXPRESSION IN A NEW HEPATOCELLULAR-CARCINOMA CELL-LINE, HEP40 - INHIBITORY ACTIONS OF VITAMIN-K
GROWTH-CONTROL AND GENE-EXPRESSION IN A NEW HEPATOCELLULAR-CARCINOMA CELL-LINE, HEP40 - INHIBITORY ACTIONS OF VITAMIN-K
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DOI：
10.1002/jcp.1041650303
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发表时间：
1995-12-01
影响因子：
5.6
通讯作者：
CARR, BI
中科院分区：
文献类型：
--
作者：
BOUZAHZAH, B;NISHIKAWA, Y;CARR, BI
描述了一个新建立的细胞系Hep 40的生长特性。发现血清介导细胞生长是绝对需要的。EGF、TGF-α和HGF在血清存在或不存在的情况下均不改变细胞生长。通过几种TGF-β家族蛋白实现细胞生长的部分抑制。使用I-125标记的TGF-β的亲和交联凝胶显示，与TGF-β敏感的Hep 3B细胞系相比，Hep 40细胞中TGF-β细胞表面II型受体显著降低。然而，在Hep 40和其他几种肝癌细胞系的培养基中加入维生素K可以完全抑制生长。维生素K的生长抑制伴随着c-myc，c-jun和凝血酶原基因转录水平的增加，与TGF-β 1蛋白的作用相反，TGF-β 1蛋白的作用导致c-myc转录水平的降低。这些数据表明，这种新的人肝癌细胞系对TGF-β的生长抑制具有部分抗性，具有独特的TGF-β受体缺陷。然而，维生素K完全抑制了生长。与维生素K相比，对TGF-β反应的不同基因表达模式表明这两种生长抑制剂通过不同的途径起作用。(C)1995 Wiley-Liss，Inc.
The growth characteristics of a newly established cell line, Hep40, derived from a human hepatoma are described. An absolute requirement was found for serum to mediate cell growth. Neither EGF, TGF-alpha, nor HGF altered cell growth in the presence or absence of serum. A partial suppression of cell growth was achieved by several TGF-beta family proteins. Affinity crosslinking gels using I-125-labeled TGF-beta showed a significant decrease in the TGF-beta cell-surface type II receptor in Hep40 cells, compared to the TGF-beta-sensitive Hep3B cell line. However, growth could be completely suppressed by addition of vitamins K to the culture medium in both Hep40 and several other hepatoma cell lines. Growth suppression by vitamins K was accompanied by an increased level of transcripts for c-myc, c-jun, and prothrombin genes, in contrast to the actions of TGF-beta 1 protein, which caused a decrease in the level of c-myc transcripts. These data show that this new human hepatoma cell line has partial resistance to growth inhibition by TGF-beta with a unique TGF-beta receptor defect. However, growth was completely suppressed by vitamins K. The differing gene expression patterns in response to TGF-beta as compared to vitamin K suggest that these two growth inhibitors act through differing pathways. (C) 1995 Wiley-Liss, Inc.