ArticleThoracic cancer2014
Identification of mutant genes with high-frequency, high-risk, and high-expression in lung adenocarcinoma.
Article in Thoracic cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Control of TGFβ signalling by ubiquitination independent function of E3 ubiquitin ligase TRIP12.Cell death & disease · 2023Article
- The oncogenic E3 ligase TRIP12 suppresses epithelial-mesenchymal transition (EMT) and mesenchymal traits through ZEB1/2.Cell death discovery · 2021Article
- E3 Ubiquitin Ligase TRIP12: Regulation, Structure, and Physiopathological Functions.International journal of molecular sciences · 2020Review
- Cancer gene mutations in congenital pulmonary airway malformation patients.ERJ open research · 2019Article
- Expression profile and prognostic values of STAT family members in non-small cell lung cancer.American journal of translational research · 2019Article
- Express: A database of transcriptome profiles encompassing known and novel transcripts across multiple development stages in eye tissues.Experimental eye research · 2018Article
- Characterization of the Role of the Malate Dehydrogenases to Lung Tumor Cell Survival.Journal of Cancer · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo identify mutant genes with high-frequency-risk-expression between lung adenocarcinoma and normal samples.
methodsThe ribonucleic acid RNA-Seq data GSE34914 and GSE37765 were downloaded from the Gene Expression Omnibus database, including 12 lung adenocarcinoma samples and six controls. All RNA-Seq reads were processed and the gene-expression level was calculated. Single nucleotide variation (SNV) was analyzed and the locations of mutant sites were recorded. In addition, the frequency and risk-level of mutant genes were calculated. Gene Ontology (GO) functional analysis was performed. The reported cancer genes were searched in tumor suppressor genes, Cancer Genes, and the Catalogue of Somatic Mutations in Cancer (COSMIC) database.
resultsThe SNV annotations of somatic mutation sites showed that 70% of mutation sites in the exon region occurred in the coding sequence (CDS). Thyroid hormone receptor interactor (TRIP)12 was identified with the highest frequency. A total of 118 mutant genes with high frequency and high-risk were selected and significantly enriched into several GO terms. No base mutation of cyclin C (CCNC) or RAB11A was recorded. At fragments per kilobase per million reads (FPKM) ≥ 56.5, reported tumor suppressor genes catenin (cadherin-associated protein), delta (CTNND)1, dual specificity phosphatase (DUSP)6, malate dehydrogenase (MDH)1 and RNA binding motif protein (RBM)5, were identified. Notably, signal transducer and activator of transcription 2 (STAT2) was the only transcription factor (TF) with high-risk mutation and its expression was detected.
conclusionFor the mutant genes with high-frequency-risk-expression, CTNND1, DUSP6, MDH1 and RBM5 were identified. TRIP12 might be a potential cancer-related gene, and expression of TF STAT2 with high-risk was detected. These mutant gene candidates might promote the development of lung adenocarcinoma and provide new diagnostic potential targets for treatment.
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