Abstract：
The present study was aimed to explore the effect of triazole on growth and viability of liver cancer cells. Cell growth was examined using the MTT test and expression of several proteins was assessed by western blotting assay. The Matrigel-coated Transwell assay was employed to examine the infiltration of cells. The data from MTT assay showed that MHCC97H and H4TG liver cancer cell viability was inhibited by triazole in a concentration-dependent manner. After treatment with 0.5, 1.0, 2.0, 4, 8, and 16 µM doses of triazole, the rate of H4TG cell viability was decreased to 96, 73, 58, 39, 29, and 28%, respectively. Treatment of MHCC97H cells with 0.5, 1.0, 2.0, 4, 8, and 16 µM doses of triazole resulted in a reduction in cell viability to 94, 70, 53, 35, 22, and 21%, respectively. Triazole treatment also led to a significant reduction in MHCC97H cell invasiveness compared to the control cells. In MHCC97H cells treated with triazole, there was a noticeable decrease in the levels of p-ERK1/2, and p-Akt protein expression. Treatment of MHCC97H cells with triazole resulted in a prominent increase in p-p38 level. In summary, triazole inhibits growth and viability of liver cancer cells through targeting the activation of p-ERK1/2 and Akt proteins. Therefore, triazole may be investigated further as a therapeutic agent for the treatment of liver cancer.
摘要：
本研究旨在探讨三唑对肝癌细胞生长和活力的影响。使用MTT测试检查细胞生长，并通过蛋白质印迹测定法评估几种蛋白质的表达。采用Matrigel包被的Transwell测定法来检查细胞的浸润。MTT分析的数据表明，三唑以浓度依赖性方式抑制MHCC97H和H4TG肝癌细胞的活力。用0.5、1.0、2.0、4、8和16µM剂量的三唑治疗后，H4TG细胞存活率下降到96、73、58、39、29和28%，分别。用0.5、1.0、2.0、4、8和16µM剂量的三唑处理MHCC97H细胞导致细胞活力降低至94、70、53、35、22和21％，分别。与对照细胞相比,三唑处理还导致MHCC97H细胞侵袭力的显著降低。在用三唑处理的MHCC97H细胞中，p-ERK1/2和p-Akt蛋白表达水平显著下降.用三唑处理MHCC97H细胞导致p-p38水平显著增加。总之,三唑通过靶向激活p-ERK1/2和Akt蛋白抑制肝癌细胞的生长和活力。因此,可以进一步研究三唑作为治疗肝癌的治疗剂。
