ArticleTranslational cancer research2022
The 1q21.3 region driver gene
Article in Translational cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 3 citations in OpenAlex.
- BCL11B predetermines a persister state in breast cancer that is reversed by TNFα.Science advances · 2026Article
- EphA3/EFNA3 Reverse Signalling Promotes Epithelial-to-Mesenchymal Transition via ERK Pathway to Facilitate Colorectal Cancer Metastasis.Digestive diseases and sciences · 2025Article
- NSUN5 accelerates the progression of liver hepatocellular carcinoma by m5C-EFNA3-mediated glycolysis.BMC cancer · 2025Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Lung adenocarcinoma (LUAD) is the leading cause of cancer deaths in the world. Therefore, it is necessary to explore the underlying mechanism of Methods: Differentially-expressed genes (DEGs) in LUAD tissues were screened based on The Cancer Genome Atlas (TCGA) database. The gene copy number variations in the 1q21.3 region were clarified by copy number variation analysis. Genes associated with overall survival (OS) were identified by Kaplan-Meier (KM) analysis. The intersection of the genes was used to obtain the driver genes. LUAD patients were grouped with driver gene expression, and the DEGs were identified. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was used to identify the enrichment pathways of the driver genes. Results: A total of 483 LUAD samples and 59 normal control samples were obtained from TCGA database, and 640 upregulated genes were identified. 154 genes with a coefficient of copy number variations greater than 10% in the 1q23.1 region and 1,247 genes that were significantly associated with patient OS were selected. The intersection results indicated that EFNA3 might be a driver gene of LUAD. KEGG enrichment analysis indicated that the DEGs were mainly enriched in apoptosis-related pathways. Cell experiments showed that after lentiviral knockdown of Conclusions: As a driver gene in the progression of LUAD,
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