NDLI: The TEAD4-DYNLL1 axis accelerates cell cycle progression and augments malignant properties of lung adenocarcinoma cells

Content Provider	Springer Nature : BioMed Central
Author	Li, Dapeng Wang, An Wang, Xuan Shi, Mengkun Chen, Xiaofeng Lyu, Yubao Huang, Dayu
Abstract	Background Lung adenocarcinoma (LUAD) is a major contributor to global mortality. Grounded onto bioinformatics insights, this study probes the functions of dynein light chain LC8-type 1 (DYNLL1) in LUAD progression. Methods DYNLL1 levels in LUAD and normal cells were determined using qPCR and western blotting analyses. Lentiviral plasmids-mediated DYNLL1 silencing was induced in LUAD cells, followed by functional assays to investigate DYNLL1’s impacts on proliferation, mobility, apoptosis, and cell cycle distribution. KY19382, a Wnt/β-catenin agonist, was employed to analyze the involvement of the Wnt/β-catenin pathway in DYNLL1’s effects. Upstream regulator of DYNLL1 was queried using bioinformatics. Mouse LUAD cells LA795 were implanted into BALB/c nude mice to establish animal tumor models. Results DYNLL1 exhibited heightened expression in LUAD cells. Its artificial silencing reduced proliferation and dissemination of cancer cells, promoted cell apoptosis, and induced G0/G1 cell cycle arrest. DYNLL1 silencing reduced β-catenin levels in cancer cells, and KY19382 treatment diminished the effects induced by DYNLL1 silencing. TEA domain transcription factor 4 (TEAD4), upregulated in LUAD cells, binds to the DUNLL1 promoter for transcriptional activation. TEAD4 silencing in LUAD cells reduced DYNLL1 transcription and β-catenin levels, thus suppressing proliferation while promoting apoptosis, senescence, and cell cycle arrest. In vivo, TEAD4 silencing weakened tumorigenesis of LA795 cells. Nevertheless, these phenomena were counteracted by the artificial DYNLL1 restoration in LUAD cells. Conclusion This investigation demonstrates a TEAD4-DYNLL1 axis that accelerates cell cycle progression and augments malignant properties of LUAD cells via the Wnt/β-catenin pathway.
Related Links	https://eurjmedres.biomedcentral.com/counter/pdf/10.1186/s40001-025-02500-y.pdf
Ending Page	14
Page Count	14
Starting Page	1
File Format	HTM / HTML
DOI	10.1186/s40001-025-02500-y
Journal	European Journal of Medical Research
Issue Number	1
Volume Number	30
Language	English
Publisher	BioMed Central
Publisher Date	2025-04-01
Access Restriction	Open
Subject Keyword	Medicine Public Health Infectious Diseases Internal Medicine Surgery Oncology Biomedicine Lung adenocarcinoma TEAD4 DYNLL1 Cell cycle Wnt/β-catenin pathway Medicine/Public Health
Content Type	Text
Resource Type	Article
Subject	Medicine
Journal Impact Factor	2.8/2023
5-Year Journal Impact Factor	2.9/2023

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1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
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