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目的观察趋化因子受体4(CXCR4)通过激活PI3K/Akt和Erk信号通路在卵巢癌SKOV3细胞上皮细胞-间充质转化(EMT)中的作用。方法 Boyden小室检测激活CXCR4后SKOV3细胞迁移和侵袭能力的变化情况。Western印迹方法检测激活CXCR4后SKOV3细胞中EMT相关蛋白的表达情况及PI3K/Akt和Erk信号通路的活化情况。PI3K/Akt和Erk信号通路抑制剂预处理SKOV3细胞后,采用Western印迹方法检测SKOV3细胞中EMT相关蛋白的表达情况。结果同对照组相比,激活CXCR4后可促进SKOV3细胞的迁移和侵袭能力(P<0.01),下调SKOV3细胞中与EMT相关的E-钙黏蛋白表达,并上调EMT相关波形蛋白的表达。Western印迹结果显示随着CXCR4刺激时间的延长,SKOV3细胞中PI3K/Akt蛋白和Erk蛋白磷酸化水平逐渐升高。采用PI3K/Akt信号通路抑制剂LY294002和Erk信号通路抑制剂U0126预处理SKOV3细胞后,CXCR4介导的E-钙黏蛋白表达下调和波形蛋白表达上调被阻断。结论 CXCR4通过激活SKOV3细胞中的PI3K/Akt信号通路和Erk信号通路,下调SKOV3细胞中E-钙黏蛋白表达,并上调波形蛋白的表达,从而促进卵巢癌SKOV3细胞EMT的发生。
AIM To investigate the role of chemokine receptor 4 (CXCR4) in the epithelial-mesenchymal transition (EMT) of ovarian cancer SKOV3 cells by activating the PI3K / Akt and Erk signaling pathways. Methods Boyden chamber was used to detect the migration and invasion ability of SKOV3 cells after activating CXCR4. Western blotting was used to detect the expression of EMT-related protein and the activation of PI3K / Akt and Erk signaling in SKOV3 cells activated by CXCR4. After SKOV3 cells were pretreated with PI3K / Akt and Erk signaling inhibitors, the expression of EMT-related proteins in SKOV3 cells was detected by Western blotting. Results Compared with the control group, CXCR4 activation promoted SKOV3 cell migration and invasion (P <0.01), down-regulated EMT-related E-cadherin expression and up-regulated EMT-associated vimentin expression in SKOV3 cells. Western blotting showed that the phosphorylation of PI3K / Akt and Erk protein in SKOV3 cells gradually increased with the increase of CXCR4 stimulation time. CXCR4-mediated downregulation of E-cadherin and up-regulation of vimentin were blocked by PI3K / Akt signaling pathway inhibitor LY294002 and Erk signaling pathway inhibitor U0126 pretreatment of SKOV3 cells. Conclusion CXCR4 can promote EMT in SKOV3 ovarian cancer cells by activating PI3K / Akt signaling pathway and Erk signaling pathway in SKOV3 cells, down-regulating E-cadherin and up-regulating the expression of vimentin in SKOV3 cells.