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在人乳腺癌细胞系MCF-7中,吡哆醛引起的生长抑制和细胞死亡依赖于p53。

Growth suppression and cell death by pyridoxal is dependent on p53 in the human breast cancer cell line MCF-7.

作者信息

Minamino Masaki, Oka Tatsuzo, Kanouchi Hiroaki

机构信息

a Joint Faculty of Veterinary Medicine, Department of Veterinary Pathobiology , Kagoshima University , Kagoshima , Japan.

出版信息

Biosci Biotechnol Biochem. 2015;79(1):124-9. doi: 10.1080/09168451.2014.952618.

DOI:10.1080/09168451.2014.952618
PMID:25603814
Abstract

Vitamin B6 compound, pyridoxine (PN), has shown antitumor action. Our previous experiments showed that PN induces expression of insulin-like growth factor binding protein-3 to arrest proliferation and induce cell death. This induction is inhibited by the p53-specific inhibitor pifithrin-α. Here, we report that another B6 compound, pyridoxal (PL), strongly inhibited MCF-7 cell growth compared to PN. PL induced the G0/G1 arrest and the accumulation of subG1 population. Although p53 mRNA was not changed by PL, 0.5 mM PL increased the protein level in MCF-7 cells. The cell growth suppression by 0.5 mM PL did not occur when p53 expression was knocked down using siRNA. Together, these data suggest that PL accumulate p53 and PL-induced cell growth suppression is dependent on p53 in MCF-7 breast cancer cells.

摘要

维生素B6化合物吡哆醇(PN)已显示出抗肿瘤作用。我们之前的实验表明,PN可诱导胰岛素样生长因子结合蛋白-3的表达,从而阻止细胞增殖并诱导细胞死亡。这种诱导作用被p53特异性抑制剂pifithrin-α抑制。在此,我们报告另一种B6化合物吡哆醛(PL)与PN相比,能强烈抑制MCF-7细胞的生长。PL诱导G0/G1期阻滞和亚G1期细胞群的积累。虽然PL不会改变p53 mRNA,但0.5 mM的PL可增加MCF-7细胞中的蛋白质水平。当使用小干扰RNA敲低p53表达时,0.5 mM PL对细胞生长的抑制作用不会发生。总之,这些数据表明PL可使p53蓄积,且PL诱导的细胞生长抑制依赖于MCF-7乳腺癌细胞中的p53。

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