目的：本研究通过检测β‐catenin蛋白在紫杉醇治疗宫颈癌过程中的表达，探讨wnt／β‐catenin信号通路在紫杉醇治疗宫颈癌中的作用机制。方法：MTT比色法检测不同浓度紫杉醇对人宫颈癌Caski细胞株增殖的影响，计算抑制率及IC50，对照组未予紫杉醇处理，而实验组则加入紫杉醇（IC50终浓度），采用细胞免疫组织化学法检测两组Caski细胞β‐catenin蛋白表达。结果：采用不同紫杉醇溶液浓度分别作用Caski细胞24h、48h及72h后，通过MTT比色法检测结果显示对细胞的抑制作用随药物浓度的增加而增强，IC50值由IC50专用计算软件求得IC50＝（6．04±1．70）nmol／L。实验组和对照组β‐catenin蛋白于胞浆胞核中均有表达，实验组β‐catenin蛋白表达阳性率为39．3％，对照组β‐catenin蛋白表达阳性率为71．7％，实验组中阳性率明显减少（P＜0．05）。紫杉醇对Caski细胞增殖的影响呈剂量效应和时间效应关系。实验组β‐catenin蛋白表达阳性率为39．3％，对照组β‐catenin蛋白表达阳性率为71．7％，实验组中阳性率明显减少（P＜0．05）。结论：单纯应用一定浓度的紫杉醇均能抑制Caski细胞的增殖。紫杉醇能够抑制宫颈癌Caski细胞内β‐catenin蛋白表达，呈浓度依赖性，从而阻断wnt／β‐catenin信号传导通路，同时影响癌基因表达，进而诱导宫颈癌Caski细胞的凋亡。%Objective :In this study ,the core protein expression changes of wnt/β‐catenin signaling pathway detected from protein levels after paclitaxel on Caski cells ,and then exploring the mechanism of the wnt/β‐catenin signaling pathway in the course of paclitaxel treatment of cervical cancer .Methods :To detect with different density of paclitaxel on the proliferation of human cervical carcinoma Caski cell by MTT colorimetric assay .Calculated inhibition ratio and IC50 .Experimental group added paclitaxel .Control group were not treated incubator .β‐catenin protein expression were detected by immunohistochemistry .Results:The inhibitory effect on the cell increase while the drug concentration in‐creased .In experimental group ,the positive rate was 39 .3% .In control group ,the positive rate was 71 .7% .The positive rate in experimental group was significantly decreased (P<0 .05) .Conclusion:The effect of Paclitaxel inhibi‐ting Caski cell is exact .Application of a certain concentration of paclitaxel merely can inhibit the proliferation of Caski cells .Paclitaxel can inhibit the expression of β‐catenin protein in cervical cancer Caski cells ,thereby blocking the wnt/β‐catenin signal transduction pathway ,and inducing apoptosis of cervical cancer Caski cell.
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