目的 探讨Yes相关蛋白（YAP）沉默对人宫颈癌（CC）SiHa细胞增殖、迁移和侵袭能力的影响。 方法 对人CC细胞株SiHa细胞进行体外培养，慢病毒YAPshRNA转染到SiHa细胞，建立稳定转染的YAP-shRNA实验组（sh-YAP组）和空载质粒对照组（对照组），采用Western blotting法检测YAP沉默效果；免疫荧光法检测2组细胞中肌动蛋白（F-actin）微丝数量及形态变化；CCK-8法、Transwell小室实验和细胞划痕实验检测2组细胞存活率、迁移及侵袭细胞数以及细胞划痕愈合率；Western blotting法检测2组细胞中上皮-间质转化（EMT）相关标记物［E钙黏蛋白（E-cadherin）和锌指转录因子（Snail）］、DNA损伤修复相关蛋白γ（γ-H2AX）和凋亡相关蛋白［c-MYC和B细胞淋巴瘤2 （Bcl-2）］蛋白表达水平。 结果 慢病毒YAPshRNA转染SiHa细胞后，SiHa细胞中YAP蛋白表达水平明显降低（P<0.05）。免疫荧光实验，YAP沉默后SiHa细胞中F-actin微丝稀疏且排列规则，细胞数量减少、细胞呈现蜷缩的状态。CCK-8法，与对照组比较，sh-YAP组培养24和48 h后SiHa细胞存活率明显降低（P<0.01）；Transwell小室实验和细胞划痕实验，与对照组比较，sh-YAP组的SiHa细胞迁移和侵袭细胞数明显减少（P<0.01），细胞划痕愈合率明显降低（P<0.05）；Western blotting法，与对照组比较，sh-YAP组细胞中E-cadherin蛋白表达水平升高（P<0.05），c-MYC、Bcl-2和γ-H2AX蛋白表达水平降低（P<0.05或P<0.01）。 结论 YAP基因沉默导致人CC SiHa细胞F-actin的解聚，并调控细胞凋亡和DNA损伤修复，可能会逆转EMT进程，从而抑制肿瘤细胞增殖和迁移。

Objective To discuss the effect of Yes-associated protein （YAP） silencing on the proliferation， migration， and invasion capabilities of the human cervical cancer （CC） SiHa cells. Methods The human CC SiHa cells were cultured in vitro， and the lentiviral YAP shRNA was transfected into the SiHa cells to establish stably transfected YAP-shRNA experimental group （sh-YAP group） and empty plasmid control group （control group）. Western blotting method was used to detect the silencing effect of YAP； immunofluorescence method was used to detect the microfilament number and morphology of actin filaments （F-actin） in the cells in both groups； CCK-8 method was used to detect the survival rates of the cells in two groups； Transwell chamber assay and wound healing assay were used to detect the numbers of migration and invasion cells and scratch healing rates of the cells in two groups； Western blotting method was used to detect the expression levels of epithelial-mesenchymal transition （EMT） markers （E-cadherin and Snail）， DNA damage repair-related proteins （γ-H2AX）， and apoptosis-related proteins ［c-MYC and B-cell lymphoma-2 （Bcl-2）］ in the cells in two groups. Results The results of lentiviral YAP shRNA transfection into SiHa cells showed that the expression level of YAP protein in the SiHa cells was significantly decreased （P<0.05）. The immunofluorescence results showed that after YAP silencing， the F-actin in SiHa cells was sparse and regularly arranged， with a reduced number of cells and a shriveled appearance. The CCK-8 results showed that compared with control group， the survival rate of the SiHa cells in sh-YAP group was significantly decreased cultured for 24 and 48 h （P<0.01）. The results of Transwell chamber assay and the wound healing assay showed that compared with control group， the numbers of migration and invasion SiHa cells in sh-YAP group were significantly decreased （P<0.01）， and the cell scratch healing rates were signifiantly decreased（P<0.05）. The Western blotting results showed that compared with control group， the expression level of E-cadherin protein in the cells in sh-YAP group was increased （P<0.05）， and the expression levels of c-MYC， Bcl-2， and γ-H2AX proteins were decreased （P<0.05 or P<0.01）. Conclusion YAP gene silencing leads to the depolymerization of F-actin in the human CC SiHa cells and regulates the apoptosis and DNA damage repair， potentially reversing the EMT process， thereby inhibiting the proliferation and migration of the tumor cells.