DCLK1 Promotes Malignancy of A549 Cell Line by Activating FAK/PI3K/AKT/mTOR Pathway
10.3971/j.issn.1000-8578.2024.23.1355
- VernacularTitle:DCLK1激活FAK/PI3K/AKT/mTOR信号通路促进A549细胞的恶性行为
- Author:
Rui YAN
1
;
Zeru XIAO
1
;
Xuying HUANG
1
;
Guangyu AN
1
;
Yang GE
1
Author Information
1. Department of Oncology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
- Publication Type:BASICRESEARCH
- Keywords:
Doublecortin-like kinase 1;
A549 cell line;
FAK/PI3K/AKT/mTOR signaling pathway;
Proliferation;
Migration and invasion
- From:
Cancer Research on Prevention and Treatment
2024;51(6):419-425
- CountryChina
- Language:Chinese
-
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.
