去乙酰化酶抑制剂对乳腺癌细胞周期作用及分子机制的探讨

摘要

Objective Study the deacetylase inhibitor MS-275 to the breast cancer MCF7 cell cycle function and the mechanism. Methos 0.5、1.0、1.5 μmol / L MS-275 affects the MCF7 cell 24 hours, observes different density MS-275 with MTT to the MCF7 cell's growth inhibitory action; flow cytometry examination cell growth and the cycle;Westernblotting examine MS-275 to the mammary gland cancer cell cycle related gene expression. Results 1.0μmol/L density MS-275 has the obvious growth inhibitory action to the MCF7 cell, and presents certain quantity effect relations, may induce the mammary gland cancer cell MCF7 mitotic cycle above the 1.0μmol/L density to hinder obviously, may strengthen the p21, p27 gene obviously the expression, reduces CCND1, the CDK4D gene expression obviously.Conclusion Certain dosage’s MS-275 suppresses breast cancer MCF7 cell’s growth, may through regulate many mitotic cycle related gene induction mammary gland cancer cell mitotic cycle to hinder, the cell hinders occurrence and p21, p27 gene expression increase and CCND1, CDK4D gene expression reduced related.%目的：研究去乙酰化酶抑制剂（MS-275）对乳腺癌细胞（MCF7）周期的作用及机制。方法0.5、1.0、1.5μmol/L MS-275作用MCF7细胞24 h，用噻唑蓝（MTT）观察不同浓度MS-275对MCF7细胞的生长抑制作用；流式细胞仪检测细胞生长及周期；Westernblotting检测MS-275对乳腺癌细胞周期相关基因的表达。结果1.0μmol/L浓度的MS-275对MCF7细胞生长有抑制作用并呈现一定的量效关系，1.0μmol/L浓度以上明显诱导阻滞乳腺癌细胞MCF7细胞周期，明显增加p21，p27基因的表达，明显降低CCND1、CDK4D基因的表达。结论一定剂量的MS-275抑制乳腺癌MCF7细胞的生长，可通过调控多个细胞周期相关基因诱导乳腺癌细胞细胞周期阻滞，细胞阻滞的发生与p21，p27基因表达的增加及CCND1、CDK4D基因表达的减少相关。