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目的:观察组蛋白去乙酰化酶抑制剂MS-275对人宫颈癌SiHa细胞增殖和凋亡的影响,并探讨其可能的机制。方法:以MS-275(0、5、10、20μmol/L)作用于人宫颈癌SiHa细胞,MTT法检测细胞的增殖,流式细胞术检测细胞的凋亡,Western blotting法检测细胞内乙酰化组蛋白H4(acetylhistone4,Ac-H4)水平,RT-PCR检测p21和p53 mRNA的表达。结果:MS-275作用后,人宫颈癌SiHa细胞增殖受到抑制、细胞凋亡增加,20μmol/L MS-275作用下,细胞增殖率仅为(13.95±8.91)%,凋亡率高达(38.38±1.78)%,显著高于其他各组(P<0.01)。MS-275作用后,细胞内Ac-H4水平增加(P<0.01),p21和p53 mRNA表达增加(均P<0.01)。结论:MS-275可抑制人宫颈癌SiHa细胞的增殖,诱导SiHa细胞凋亡;上调p21和p53表达、提高组蛋白乙酰化水平可能是其作用机制之一。
Objective: To observe the effect of histone deacetylase inhibitor MS-275 on the proliferation and apoptosis of human cervical cancer SiHa cells and to explore its possible mechanism. METHODS: Human cervical cancer SiHa cells were treated with MS-275 (0, 5, 10 and 20 μmol / L). Cell proliferation was detected by MTT assay. Apoptosis was detected by flow cytometry. The expression of p21 and p53 mRNA was detected by RT-PCR. RESULTS: After treated with MS-275, the proliferation of SiHa cells was inhibited and the apoptosis rate was increased. Under the action of 20μmol / L MS-275, the cell proliferation rate was (13.95 ± 8.91)% and the apoptosis rate was as high as (38.38 ± 1.78)%, significantly higher than other groups (P <0.01). After MS-275 treatment, the level of Ac-H4 increased (P <0.01) and the expression of p21 and p53 mRNA increased (all P <0.01). Conclusion: MS-275 can inhibit the proliferation of SiHa cells and induce the apoptosis of SiHa cells. Upregulating the expression of p21 and p53 and increasing the histone acetylation levels may be one of its mechanisms.