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目的明确表皮生长因子受体(EGFR)活化参与胰腺癌细胞解离调节的分子机制。方法通过免疫荧光法检测仓鼠高转移株(PC-1.0)和低转移株(PC-1)胰腺癌细胞中EGFR、活化(磷酸化)EGFR(p-EGFR)、活化(磷酸化)丝裂原活化蛋白激酶激酶2(p-MEK1/2)及活化(磷酸化)细胞外信号调节激酶1/2(p-ERK1/2)的表达变化及其与胰腺癌细胞解离状态变化的关系。结果胰腺癌细胞解离因子(DF)明显诱导低转移株胰腺癌细胞(PC-1)中EGFR、p-EGFR、p-MEK1/2和p-ERK1/2的表达,同时诱导其细胞克隆解离。相反,AG1478(EGFR活化抑制剂)明显抑制高转移株胰腺癌细胞(PC-1.0)中EGFR、p-EGFR、p-MEK1/2和p-ERK1/2的表达,同时诱导PC-1.0细胞聚集成细胞克隆。结论表皮生长因子受体活化后激活MEK/ERK信号通路,从而参与胰腺癌细胞解离的调节。
Objective To clarify the molecular mechanism of the activation of epidermal growth factor receptor (EGFR) involved in the regulation of pancreatic cancer cell dissociation. Methods The expressions of EGFR, p-EGFR (p-EGFR), activated (phosphorylated) mitogens in PC-1.0 and PC-1 pancreatic cancer cells were detected by immunofluorescence staining. The expression of p-MEK1 / 2 and p-ERK1 / 2 and its relationship with the dissociation status of pancreatic cancer cells were determined. Results The pancreatic cancer cell dissociation factor (DF) significantly induced the expression of EGFR, p-EGFR, p-MEK1 / 2 and p-ERK1 / 2 in low metastatic pancreatic cancer cells from. In contrast, AG1478 (EGFR activation inhibitor) significantly inhibited the expression of EGFR, p-EGFR, p-MEK1 / 2 and p-ERK1 / 2 in PC-1.0 cells and induced the aggregation of PC-1.0 cells Into cell clones. Conclusion The activation of epidermal growth factor receptor activates the MEK / ERK signaling pathway and thus participates in the regulation of pancreatic cancer cell dissociation.