ArticlePeerJ2022
DDX17 modulates the expression and alternative splicing of genes involved in apoptosis and proliferation in lung adenocarcinoma cells.
Article in PeerJ, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- DDX17 and viral infection.Virulence · 2026Review
- ZNF200 and DDX17 regulatory loop promotes tumor growth and metastasis by activating RBPJ transcription in non-small cell lung cancer.Science China. Life sciences · 2026Article
- Diagnostic Biomarkers and Targeted Drug Prediction for Acute Kidney Injury: A Computational ApproachEndocrine, metabolic & immune disorders drug targets · 2026Article
- DTMUV upregulates DDX17 expression to facilitate viral replication.Veterinary research · 2025Article
- [Silencing DDX17 inhibits proliferation and migration of pulmonary arterial smooth muscle cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- METTL3 stabilizes DDX17 mRNA via IGF2BP2-mediated m6A modification to suppress endometrial cancer progression.Clinical and experimental medicine · 2025Article
- TDP-43 toxic gain of function links ALS, FTD and Alzheimer's Disease through splicing dysregulation.bioRxiv : the preprint server for biology · 2025Article
- The advances of DEAD-box RNA helicase 17 in chronic non-infectious diseases.Frontiers in cardiovascular medicine · 2025Review
- Identification of related-genes of T cells in lung tissue of chronic obstructive pulmonary disease based on bioinformatics and experimental validation.Scientific reports · 2024Article
- DEAD-Box Helicase 17 Promotes Amyloidogenesis by Regulating BACE1 Translation.Brain sciences · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The DEAD-box RNA-binding protein (RBP) DDX17 has been found to be involved in the tumorigenesis of many types of cancers. However, the role of DDX17 in lung adenocarcinoma (LUAD) remains unclear. Methods: We silenced DDX17 expression in A549 LUAD cells by small interfering RNA (siRNA). Cell proliferation and apoptosis assays were performed to explore the functions of DDX17. Knockdown of DDX17 by siRNA significantly inhibited proliferation and induced apoptosis in A549 cells. We used high-throughput RNA sequencing (RNA-seq) to identify differentially expressed genes (DEGs) and alternative splicing (AS) events in DDX17 knockdown LUAD cells. Results: DDX17 knockdown increased the expression levels of proapoptotic genes and decreased those of proproliferative genes. Moreover, the DDX17-regulated AS events in A549 cells revealed by computational analysis using ABLas software were strongly validated by quantitative reverse transcription-polymerase chain reaction (RT-qPCR) and were also validated by analysis of The Cancer Genome Atlas (TCGA)-LUAD dataset. These findings suggest that DDX17 may function as an oncogene by regulating both the expression and AS of proliferation- and apoptosis-associated genes in LUAD cells. Our findings may offer new insights into understanding the molecular mechanisms of LUAD and provide a new therapeutic direction for LUAD.
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