甲氨酰黄和孔雀石绿在大鼠肝癌发生过程中的促瘤作用与细胞周期调节蛋白的表达失调有关。

Sanjay Gupta, Monisha Sundarrajan, K V K Rao
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引用次数: 67

摘要

金属黄(MY)和孔雀石绿(MG)是纺织染料,尽管有禁令,但它们仍被用作食品着色剂。MY和MG对n -亚硝基二乙胺(DEN)诱导的肝脏肿瘤前病变有促进作用。促肿瘤药物不具有诱变性,但可能改变其产物与过度增殖、组织重塑和炎症相关的基因的表达。细胞周期控制通常的功能是确保基因组的完整性,并在G1/S或G2/M检查点阻止细胞,直到所有先决条件事件完成。为了了解MY和MG促进肿瘤的机制,我们研究了细胞增殖和细胞周期调节蛋白cyclin D1及其相关激酶cdk4、cyclin B1和相关激酶cdc2的水平。免疫组织化学染色显示,DEN治疗后给予MY和MG的动物的PCNA水平升高。Western和Northern杂交显示,与未治疗或DEN对照组相比,在给予DEN后给予MY和MG的大鼠肝脏中,细胞周期蛋白D1及其相关激酶cdk4和细胞周期蛋白B1及其相关激酶cdc2的表达均有所增加。mRNA水平的增加是由于这些基因的转录速率增加,这是通过运行转录试验研究的。通过肝脏肿瘤发展的体内模型获得的这些数据提供了强有力的证据,证明细胞周期两个关键检查点的失调与孔雀石绿和金属黄促进肿瘤的可能机制之一有关。
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Tumor promotion by metanil yellow and malachite green during rat hepatocarcinogenesis is associated with dysregulated expression of cell cycle regulatory proteins.

Metanil yellow (MY) and malachite green (MG) are textile dyes, which, despite a ban, are used as food-coloring agents. MY and MG have promoter effects on the development of hepatic preneoplastic lesions induced by N-nitrosodiethylamine (DEN). Tumor-promoting agents are not mutagenic but may alter the expression of genes whose products are associated with hyper-proliferation, tissue remodeling, and inflammation. Cell cycle controls normally function to ensure the integrity of the genome and arrest of cells at G1/S or G2/M checkpoints until all the prerequisite events are completed. In order to understand the mechanism(s) of tumor promotion by MY and MG, we have studied the levels of PCNA, a marker of cell proliferation and cell cycle regulatory proteins, cyclin D1, and its associated kinase, cdk4, cyclin B1, and associated kinase, cdc2. Immunohistochemical staining showed an elevated level of PCNA in animals administered MY and MG subsequent to DEN treatment. Western and Northern blot hybridization showed an increased expression of both cyclin D1 and its associated kinase cdk4, and cyclin B1 and its associated kinase cdc2, in livers of rats administered MY and MG after administration of DEN as compared to untreated or DEN controls. The increased level of mRNA was due to the increased rate of transcription of these genes as studied by run-on transcription assay. These data obtained by the in vivo model of liver tumor development provide strong evidence for a link between dysregulation of the two critical checkpoints of the cell cycle as one of the possible mechanism(s) during tumor promotion by malachite green and metanil yellow.

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