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HSP90抑制剂作为新型抗肿瘤药物,其治疗肿瘤效果良好,是目前抗肿瘤新药研发的热点。本研究目的在于探讨Hsp90特异性抑制剂对宫颈癌hela细胞增殖、凋亡影响及其调节p53通路的作用机制。利用HSP90抑制剂干预宫颈癌hela细胞24 h、48 h、72 h后细胞生长抑制率情况,观察HSP90抑制剂作用宫颈癌hela细胞48 h后细胞凋亡及半胱氨酸蛋白酶-3(Caspase-3)、半胱氨酸蛋白酶-8(Caspase-8)及p53蛋白水平变化的影响。结果表明,HSP90抑制剂可导致宫颈癌hela细胞形态学改变,增加细胞通透性,破坏细胞膜导致细胞破碎脱落。HSP90抑制剂能有效抑制宫颈癌hela细胞,可抑制细胞增殖并促进宫颈癌hela细胞凋亡,且呈剂量及时间依赖性。在细胞培养48 h后随HSP90抑制剂浓度增加,Caspase-3、Caspase-8、p53表达显著增加。结果表明HSP90抑制剂能可通过上调Caspase-3、Caspase-8、p53蛋白表达而诱导宫颈癌hela细胞凋亡。
As a new anti-tumor drug, HSP90 inhibitor has good therapeutic effect on tumor and is a hot spot in the development of new antitumor drug. The purpose of this study is to investigate the effect of Hsp90-specific inhibitor on proliferation and apoptosis of cervical cancer hela cells and its mechanism of regulating p53 pathway. The effect of HSP90 inhibitor on the cell growth inhibition rate of hela cells in 24 h, 48 h and 72 h was observed. The apoptosis of Hela cells and the expression of Caspase- 3), Caspase-8 and p53 protein levels. The results showed that, HSP90 inhibitors can cause cervical cancer hela cells morphological changes, increase cell permeability, destruction of the cell membrane lead to cell broken off. HSP90 inhibitor can effectively inhibit hela cells in cervical cancer, inhibit cell proliferation and promote apoptosis of hela cells in a dose-and time-dependent manner. After 48 h of culture, the expression of Caspase-3, Caspase-8 and p53 increased significantly with the increase of HSP90 concentration. The results show that HSP90 inhibitor can induce apoptosis of cervical cancer hela cells by up-regulating Caspase-3, Caspase-8 and p53 protein expression.