Growth inhibition of both MCF-7 and Hs578T human breast cancer cell lines by vitamin D analogues is associated with increased expression of insulin-like growth factor binding protein-3
Growth inhibition of both MCF-7 and Hs578T human breast cancer cell lines by vitamin D analogues is associated with increased expression of insulin-like growth factor binding protein-3
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DOI：
10.1677/jme.0.0200157
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发表时间：
1998-02-01
影响因子：
3.5
通讯作者：
Holly, JMP
中科院分区：
文献类型：
--
作者：
Colston, KW;Perks, CM;Holly, JMP
研究了两种维生素D类似物EB1089和CB1093在MCF-7和Hs578T人乳腺癌细胞株中对胰岛素样生长因子结合蛋白（IGFBP）表达的影响。Western-ligand blotting发现，两种维生素D类似物均抑制igf - 1，刺激MCF-7细胞生长，并增强IGFBP-3的产生。重组人IGFBP-3在1 ~ 235 ng/ml浓度范围内抑制MCF-7细胞的生长。Hs578T细胞对igf - 1的有丝分裂作用无反应，但生长受到两种维生素D类似物的抑制。用EB1089和CB1093 （10 nM）以及100 nM的9-顺式维甲酸（9-顺式RA）或全反式维甲酸（ATRA）处理Hs578T细胞与条件培养基中IGFBP-3的积累增加相关。此外，通过Western配体印迹和放射免疫分析评估，EB1089和9-顺式RA共处理Hs578T细胞可增强条件培养基中细胞生长和IGFBP-3积累的抑制作用。这些发现表明IGFBP-3在维生素D类似物的生长抑制作用中起作用。
The effects of two vitamin D analogues, EB1089 and CB1093, on insulin-like growth factor binding protein (IGFBP) expression have been examined in MCF-7 and Hs578T human breast cancer cell lines. Both vitamin D analogues inhibited IGF-I stimulated growth of MCF-7 cells and enhanced the production of IGFBP-3 as determined by Western-ligand blotting. Recombinant human IGFBP-3 inhibited the growth of MCF-7 cells over the concentration range 1-235 ng/ml. Hs578T cells were unresponsive to the mitogenic effects of IGF-I but growth was inhibited by the two vitamin D analogues. Treatment of Hs578T cells with EB1089 and CB1093 (10 nM) as well as 100 nM 9-cis retinoic acid (9-cis RA) or all-trans retinoic acid (ATRA) was associated with increased accumulation of IGFBP-3 in conditioned medium. Furthermore, cotreatment of Hs578T cells with EB1089 and 9-cis RA led to augmented effects on both inhibition of cell growth and IGFBP-3 accumulation in conditioned medium as assessed by Western ligand blotting and radioimmunoassay. These findings suggest a role for IGFBP-3 in the growth inhibitory effects of vitamin D analogues.