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目的研究组蛋白去乙酰酶抑制剂-曲古菌素A(TSA)对乳腺癌T47D细胞增殖的影响和机制。方法不同浓度的TSA作用乳腺癌T47D细胞5 d,噻唑蓝(MTT)法检测药物作用前后细胞增殖的情况。流式细胞仪检测TSA作用36 h后细胞周期的改变。逆转录-聚合酶链反应(RT- PCR)检测TSA作用36 h后Maspin mRNA的表达。结果TSA在20μg/L浓度以上可以明显抑制乳腺癌T47D细胞的增殖,并呈现剂量和时间的依赖性。细胞周期检测发现100μg/L TSA可导致细胞G_1期阻滞,并诱导细胞凋亡;而500μg/L TSA可显著的诱导细胞凋亡。RT-PCR显示100μg/ L TSA作用36 h后Maspin mRNA的表达增强,但在20μg/L时其表达与对照组差异无统计学意义。结论TSA可以抑制乳腺癌T47D细胞的生长,可能通过诱导细胞凋亡和Maspin基因的重新表达发挥抑癌作用。TSA可能是乳腺癌治疗的潜在靶点。
Objective To study the effect of histone deacetylase inhibitor trichostatin A (TSA) on the proliferation of breast cancer T47D cells and its mechanism. Methods T47D cells were treated with different concentrations of TSA for 5 days. The proliferation of breast cancer cells was detected by MTT assay. Flow Cytometry TSA role in the cell cycle after 36 h change. The expression of Maspin mRNA was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) 36 h after TSA treatment. Results TSA at a concentration of 20μg / L could significantly inhibit the proliferation of breast cancer T47D cells in a dose-and time-dependent manner. Cell cycle assay showed that 100μg / L TSA could induce G1 phase arrest and induce cell apoptosis, while 500μg / L TSA induced cell apoptosis significantly. The expression of Maspin mRNA was enhanced after treated with 100μg / L TSA for 36h, but no significant difference was found between the expression of Maspin mRNA and control group at 20μg / L RT-PCR. Conclusions TSA can inhibit the growth of breast cancer T47D cells and may play a role of tumor suppressor by inducing apoptosis and re-expressing Maspin gene. TSA may be a potential target for the treatment of breast cancer.