肿瘤防治研究2024，Vol.51Issue(6)：419-425,7.DOI:10.3971/j.issn.1000-8578.2024.23.1355
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
摘要
Abstract
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Key words
Doublecortin-like kinase 1/A549 cell line/FAK/PI3K/AKT/mTOR signaling pathway/Prolifer-ation/Migration and invasion分类
医药卫生引用本文复制引用
闫锐,肖泽儒,黄旭颖,安广宇,葛洋..DCLK1激活FAK/PI3K/AKT/mTOR信号通路促进A549细胞的恶性行为[J].肿瘤防治研究,2024,51(6):419-425,7.基金项目
National Natural Science Foundation of China-Youth Foundation(No.82303649) （No.82303649）
Golden Seed Project of Beijing Chao-Yang Hospital,Capital Medical University(No.CYJZ202226) 国家自然科学基金-青年项目(82303649) （No.CYJZ202226）
首都医科大学附属北京朝阳医院金种子项目(CYJZ202226) （CYJZ202226）
