摘要： 目的 探讨Src酪氨酸激酶抑制剂对表皮生长因子（EGF）诱导的肺腺癌细胞生长浸润的作用及其机制。方法 选用PC-9和A549细胞进行培养，分别给予不同浓度的Src酪氨酸激酶抑制剂和EGF，利用MTT比色法和Boyden-chamber法检测PC-9和A549细胞增殖及浸润情况，台盼蓝染色检测细胞活力，蛋白质印迹检验Src蛋白的表达和磷酸化及其下游信号磷酸化情况。结果 抑制Src酪氨酸激酶可以在不影响细胞活力的情况下抑制PC-9和A549细胞的增殖浸润，EGF可以增强EGF受体（EGFR）、Src、促丝裂原活化蛋白激酶（MAPK）及Akt的磷酸化，Src酪氨酸激酶抑制剂可以抑制这种磷酸化。结论 抑制Src酪氨酸激酶可以通过调节EGFR及其下游信号通路抑制肺腺癌细胞的增殖浸润。

Src酪氨酸激酶抑制剂对表皮生长因子诱导的肺腺癌细胞生长的作用及机制

张鹤, 赵晓宇, 郑锐, 何忠

中国医科大学附属盛京医院呼吸与危重症医学科, 沈阳 110022

收稿日期:2022-09-30出版日期:2023-02-28发布日期:2023-02-04
通讯作者:何忠E-mail:hez1@sj-hospital.org
作者简介:张鹤(1988-),女,医师,硕士.
基金资助:辽宁省重点研发计划（2018225006，2020JH2/10300125）


关键词: Src酪氨酸激酶抑制剂, 表皮生长因子受体, Src, 肺腺癌
Abstract: Objective To explore the mechanism of Src tyrosine kinase inhibiting phosphorylation of EGFR and its downstream signaling in non-small cell lung cancer. Methods PC-9 and A549 cells were cultured with different concentrations of Src-TKI. The invasion and proliferation of PC-9 and A549 were measured using MTT and Boyden chamber. Cell viability was estimated using the Trypan blue exclusion test. Src expression and Src-TKI-mediated inhibition of Src phosphorylation were assayed using Western blotting. Results Src-TKI can inhibit proliferation and invasion of A549 and PC-9 induced by EGF without influencing cell viability. EGF can enhance the phosphorylation of EGFR, Src, MAPK and Akt. Src-TKIs can suppress the phosphorylation of EGFR, Src, MAPK and Akt induced by EGF. Conclusion Src-TKI can suppress the growth of NSCLC by regulating EGFR and its downstream signaling.
Key words: Src tyrosin kinase inhibitor, epidermal growth factor receptor, Src, non-small cell lung cancer
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