DCLK1激活FAK/PI3K/AKT/mTOR信号通路促进A549细胞的恶性行为  

DCLK1 Promotes Malignancy of A549 Cell Line by Activating FAK/PI3K/AKT/mTOR Pathway

作　　者：闫锐[1] 肖泽儒 黄旭颖 安广宇[1] 葛洋[1] YAN Rui;XIAO Zeru;HUANG Xuying;AN Guangyu;GE Yang(Department of Oncology,Beijing Chaoyang Hospital,Capital Medical University,Beijing 100020,China)

机构地区：[1]首都医科大学附属北京朝阳医院肿瘤科,北京100020

出　　处：《肿瘤防治研究》2024年第6期419-425,共7页Cancer Research on Prevention and Treatment

基　　金：国家自然科学基金-青年项目(82303649);首都医科大学附属北京朝阳医院金种子项目(CYJZ202226)。

摘　　要：目的探讨双肾上腺素皮质样激酶1(DCLK1)对A549细胞增殖、迁移、侵袭等恶性生物学行为的影响,并探究可能涉及的相关分子机制。方法慢病毒感染法建立稳定表达DCLK1分子的A549细胞系,反转录-聚合酶链技术和蛋白质印记法进行鉴定。CCK-8与平板克隆实验检测过表达DCLK1后细胞增殖能力变化。Transwell实验观察过表达DCLK1对细胞迁移与侵袭能力的影响。癌症基因组图谱(TCGA)数据库分析DCLK1对肺腺癌细胞的调控富集通路,蛋白质印记法进行验证。结果DCLK1在A549细胞中过表达可增加细胞的增殖、迁移与侵袭等能力,而抑制FAK/PI3K/AKT/mTOR信号通路可削弱DCLK1对A549细胞的恶性调控。结论DCLK1通过激活FAK/PI3K/AKT/mTOR信号通路,促进A549细胞的恶性生物学行为。Objective To investigate the effects of doublecortin-like kinase 1(DCLK1)on the malignant biological behaviors,such as proliferation,migration,and invasion,of A549 cell line and their corresponding mechanisms.Methods DCLK1-overexpressing A549 cell lines were established through lentiviral infection,and DCLK1 expression was validated by using RT-PCR and Western blot analysis.Proliferation ability was assessed with CCK-8 and plate cloning assays,and migration and invasion abilities were examined with Transwell assays.The pathway regulated by DCLK1 in lung adenocarcinoma was analyzed on the basis of the TCGA lung adenocarcinoma cohort with pathway enrichment analysis and verified through Western blot analysis.Results DCLK1 overexpression in A549 cells promoted cell proliferation,migration,and invasion.The inhibition of the FAK/PI3K/AKT/mTOR signaling pathway impaired the DCLK1-mediated malignant behavior of A549 cells.Conclusion DCLK1 promotes the malignant behavior of A549 cells through the activation of the FAK/PI3K/AKT/mTOR signaling pathway.

关 键 词：双肾上腺素皮质样激酶1 A549细胞系 FAK/PI3K/AKT/mTOR信号通路 增殖 迁移与侵袭 

分 类 号：R734[医药卫生—肿瘤]