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目的探讨JAK2/STAT3通路在表皮生长因子(epidermal growth factor,EGF)诱导结肠癌细胞侵袭迁移中的作用。方法以人结肠癌细胞株LoVo为研究对象,分为对照组、表皮生长因子处理组(EGF组)、表皮生长因子与JAK2激酶抑制剂AG490共处理组(EGF+AG490组)。采用免疫荧光和Western blot检测各组LoVo细胞E钙粘素蛋白、磷酸化STAT3表达水平;Transwell法检测细胞侵袭能力;细胞划痕实验检测细胞迁移能力。结果细胞划痕实验对照组细胞划痕闭合约38%,EGF+AG490组细胞划痕闭合约40%,而EGF组闭合约80%。EGF组显著高于另2组(P<0.05);体外侵袭实验显示对照组透膜细胞数为(21.24±2.65)/视野,EGF+AG490组为(23.19±3.50)/视野,EGF组为(55.08±2.14)/视野。EGF组显著高于另2组(P<0.05);与EGF+AG490组结肠癌LoVo细胞相比,EGF组细胞P-STAT3表达增加72.4%,E-cadherin蛋白表达降低68.5%(P<0.05);免疫荧光显示EGF组细胞E-cadherin向细胞质内移位。结论EGF可通过JAK2/STAT3通路调节E-cadherin在结肠癌LoVo细胞中的表达和定位,增强结肠癌细胞的侵袭迁移能力。
Objective To investigate the role of JAK2 / STAT3 pathway in the invasion and migration of colon cancer cells induced by epidermal growth factor (EGF). Methods Human colon cancer cell line LoVo was divided into control group, epidermal growth factor treatment group (EGF group), epidermal growth factor and JAK2 kinase inhibitor AG490 co-treatment group (EGF + AG490 group). Immunofluorescence and Western blot were used to detect the expression of E-cadherin and phosphorylated STAT3 in LoVo cells. Transwell assay was used to detect cell invasion ability. Cell scratch assay was used to detect cell migration. RESULTS: Scratches in cells of the control group were approximately 38% scratched in the cell scratch test. Scratches in the EGF + AG490 group were approximately 40% scratched, while the EGF group was closed approximately 80%. The EGF group was significantly higher than the other two groups (P <0.05). In vitro invasion assay showed that the number of transmembrane cells in the control group was (21.24 ± 2.65) / field, EGF + AG490 group was (23.19 ± 3.50) / field, 55.08 ± 2.14) / field of view. (P <0.05). Compared with EGF + AG490 group, the expression of P-STAT3 increased 72.4% and the expression of E-cadherin decreased by 68.5% (P <0.05) Immunofluorescence showed that E-cadherin in EGF group translocated to the cytoplasm. Conclusion EGF can regulate the expression and localization of E-cadherin in colon cancer LoVo cells through JAK2 / STAT3 pathway and enhance the invasion and migration of colon cancer cells.