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Antitumor Molecular Mechanism of Chlorogenic Acid on Inducting Genes GSK-3βand APC and Inhibiting Geneβ-Catenin

机译:绿原酸对诱导基因GSK-3β和APC及抑制基因β-连环蛋白的抗肿瘤分子机理

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Objective.Inhibiting geneβ-catenin and inducting genes GSK-3βand APC, promoting the tumor cell apoptosis in Wnt pathway, by chlorogenic acid were discussed (CGA).Method.The different genes were scanned by the 4*44K mouse microarray chips. The effect of the three genes was confirmed by RT-PCR technique with CGA dosage of 5, 10, and 20 mg/kg.Result.The expression of GSK-3βand APC was upregulated in group of 20 mg/kg dosage (P<0.05) and the expression ofβ-catenin was downregulated in the same dosage (P<0.05).Conclusion.The results infer that the multimeric protein complex ofβ-catenin could be increased by CGA upregulated genes GSK-3βand APC, which could inhibit the freeβ-catenin into the nucleus to connect with TCF. So the transcriptional expression of the target genes will be cut to abnormal cell proliferation. It is probably one of the ways that can stop the tumor increase by CGA.
机译:目的:探讨利用绿原酸(CGA)抑制β-catenin基因,诱导基因GSK-3β和APC,促进Wnt通路中肿瘤细胞凋亡的方法。用4×44K小鼠微阵列芯片扫描不同基因。 RT-PCR技术证实了这三个基因的作用,CGA剂量分别为5、10和20μmg/ kg。结果。20μmg/ kg剂量组GSK-3β和APC的表达上调(P <0.05结论相同剂量下β-catenin的表达下调(P <0.05)。结论:CGA上调基因GSK-3β和APC可增加β-catenin的多聚体蛋白复合物,抑制游离β-连环蛋白进入细胞核与TCF连接。因此,靶基因的转录表达将被切割为异常细胞增殖。这可能是通过CGA阻止肿瘤增长的方法之一。

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