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目的:探讨CDC42抑制剂ML141对喉癌细胞增殖的抑制作用,为喉癌的分子治疗提供新的靶点。方法:体外培养人喉癌Hep-2细胞。实时定量聚合酶链反应(Real-time PCR)检测CDC42在Hep-2细胞中的表达。利用GLISA法检测ML141对CDC42活性的抑制效果。利用CCK8法检测ML141对Hep-2细胞增殖能力的抑制效果。结果:1Real-time PCR结果显示在人喉癌Hep-2细胞中CDC42显著高表达(P<0.001),证明全基因组的结果准确。2GLISA结果显示表皮生长因子作用的Hep-2细胞中CDC42的活性明显高表达,但加入ML141的Hep-2细胞中CDC42的活性受到明显抑制。(P<0.001)。3CCK8结果显示24 h,48h和72 h时,ML141处理的Hep-2细胞的增殖能力与对照组相比均受到明显抑制。(P<0.001)。结论:促癌基因CDC42抑制剂ML141能够抑制人喉癌Hep-2细胞增殖,具有成为抗喉癌新药的潜力,为喉癌的分子治疗提供新的切入点。
Objective: To investigate the inhibitory effect of ML141, a CDC42 inhibitor, on the proliferation of laryngeal carcinoma cells and to provide a new target for the molecular therapy of laryngeal carcinoma. Methods: Human laryngeal carcinoma Hep-2 cells were cultured in vitro. Real-time quantitative polymerase chain reaction (Real-time PCR) CDC42 expression in Hep-2 cells. The inhibitory effect of ML141 on CDC42 activity was tested by GLISA. The inhibitory effect of ML141 on the proliferation of Hep-2 cells was detected by CCK8 assay. Results: Real-time PCR results showed that CDC42 was highly expressed in human laryngeal carcinoma Hep-2 cells (P <0.001), which showed that the whole genome was accurate. The results of 2GLISA showed that the activity of CDC42 in Hep-2 cells was significantly higher than that of the epidermal growth factor, but the activity of CDC42 in Hep-2 cells with ML141 was significantly inhibited. (P <0.001). 3CCK8 results showed that the proliferation ability of ML141-treated Hep-2 cells was significantly inhibited compared with the control group at 24 h, 48 h and 72 h. (P <0.001). CONCLUSION: ML141, a tumor suppressor gene CDC42 inhibitor, can inhibit the proliferation of human laryngeal carcinoma Hep-2 cells and has the potential of being a new drug against laryngeal cancer, providing a new entry point for the molecular therapy of laryngeal cancer.