大黄素在dmba诱导的叙利亚金仓鼠口腔癌发生过程中下调细胞增殖标志物。

Asokan Manimaran, Rajamanickam Buddhan, Shanmugam Manoharan
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引用次数: 13

摘要

背景:细胞周期破坏是肿瘤转化的主要特征,因此细胞周期调节因子的状态可以用来评估癌症患者的预后意义。采用PCNA、细胞周期蛋白D1、CDK4、CDK6和survivin在口腔黏膜中的表达,评价大黄素对7,12-二甲基苯(a)蒽(DMBA)诱导的叙利亚金仓鼠口腔癌变过程中异常细胞增殖的影响。材料与方法:局部应用DMBA,每周3次,连续14周,用于发生分化良好的鳞状细胞癌的仓鼠颊袋。结果:单用DMBA处理的仓鼠口腔黏膜细胞周期蛋白D1和PCNA过表达,CDK4、CDK6和survivin表达上调。口服大黄素(50mg/kg b.w)可下调DMBA处理仓鼠口腔黏膜细胞增殖标志物的表达。结论:大黄素的抗细胞增殖作用可能是通过调节细胞周期标志物抑制DMBA诱导的口腔癌。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

EMODIN DOWNREGULATES CELL PROLIFERATION MARKERS DURING DMBA INDUCED ORAL CARCINOGENESIS IN GOLDEN SYRIAN HAMSTERS.

EMODIN DOWNREGULATES CELL PROLIFERATION MARKERS DURING DMBA INDUCED ORAL CARCINOGENESIS IN GOLDEN SYRIAN HAMSTERS.

EMODIN DOWNREGULATES CELL PROLIFERATION MARKERS DURING DMBA INDUCED ORAL CARCINOGENESIS IN GOLDEN SYRIAN HAMSTERS.

EMODIN DOWNREGULATES CELL PROLIFERATION MARKERS DURING DMBA INDUCED ORAL CARCINOGENESIS IN GOLDEN SYRIAN HAMSTERS.

Background: Cell-cycle disruption is the major characteristic features of neoplastic transformation and the status of cell-cycle regulators can thus be utilized to assess the prognostic significance in patients with cancer. The PCNA, cyclin D1, CDK4, CDK6 and survivin expression in the buccal mucosa was utilized to evaluate the Emodin efficacy on abnormal cell proliferation during 7,12-dimethylbenz(a)anthracene (DMBA) induced oral carcinogenesis in golden Syrian hamsters.

Materials and methods: Topical application of DMBA, three times a week for 14 weeks, on the hamsters' buccal pouches developed well differentiated squamous cell carcinoma.

Results: Cyclin D1 and PCNA over-expression and up-regulation of CDK4, CDK6 and survivin were noticed in the buccal mucosa of hamsters treated with DMBA alone. Emodin administration (50mg/kg b.w) orally to hamsters treated with DMBA down-regulated the expression of cell proliferation markers in the buccal mucosa.

Conclusions: The anti-cell proliferative role of Emodin is owing to its modulating efficacy on cell-cycle markers towards the tumor suppression during DMBA induced oral carcinogenesis.

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