ArticlePeerJ2019
Identification of key genes in non-small cell lung cancer by bioinformatics analysis.
Article in PeerJ, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- Quercetin-Fe nanodots inhibit cervical cancer cell proliferation by targeting PCNA.Cancer nanotechnology · 2026Article
- The role of miR-21 in early-stage lung adenocarcinoma: clinical and bioinformatics insights.Scientific reports · 2025Article
- Combining serum CDK1 with tumor markers for the diagnosis of small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- Up-Regulation of MELK Promotes Cell Growth and Invasion by Accelerating G1/S Transition and Indicates Poor Prognosis in Lung Adenocarcinoma.Molecular biotechnology · 2025Article
- DNA methylation biomarker analysis from low-survival-rate cancers based on genetic functional approaches.Frontiers in bioinformatics · 2025Article
- Article
- Identification of Potential Key Genes and Prognostic Biomarkers of Lung Cancer Based on Bioinformatics.BioMed research international · 2023Article
- Transcriptomic analysis reveals the potential biological mechanism of AIS and lung adenocarcinoma.Frontiers in neurology · 2023Article
- Interfering withAnnals of translational medicine · 2022Article
- CDK1 and HSP90AA1 Appear as the Novel Regulatory Genes in Non-Small Cell Lung Cancer: A Bioinformatics Approach.Journal of personalized medicine · 2022Article
- Proliferating cell nuclear antigen clamp associated factor, a potential proto-oncogene with increased expression in malignant gastrointestinal tumors.World journal of gastrointestinal oncology · 2021Review
- Peripheral blood transcriptome heterogeneity and prognostic potential in lung cancer revealed by RNA-Seq.Journal of cellular and molecular medicine · 2021Article
- KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway.Journal of experimental & clinical cancer research : CR · 2021Article
- Identification of Significant Genes in Lung Cancer of Nonsmoking Women via Bioinformatics Analysis.BioMed research international · 2021Article
- Bioinformatics analysis and experimental validation of TTK as a biomarker for prognosis in non-small cell lung cancer.Bioscience reports · 2020Article
- Estimation of Hub Genes and Infiltrating Immune Cells in Non-Smoking Females with Lung Adenocarcinoma by Integrated Bioinformatic Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- NUCKS1 Promotes Proliferation, Invasion and Migration of Non-Small Cell Lung Cancer by Upregulating CDK1 Expression.Cancer management and research · 2020Article
- Bioinformatics Analysis of Key Genes and circRNA-miRNA-mRNA Regulatory Network in Gastric Cancer.BioMed research international · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-small cell lung cancer (NSCLC) is one of the most common malignant tumors in the world, and it has become the leading cause of death of malignant tumors. However, its mechanisms are not fully clear. The aim of this study is to investigate the key genes and explore their potential mechanisms involving in NSCLC.
methodsWe downloaded gene expression profiles GSE33532, GSE30219 and GSE19804 from the Gene Expression Omnibus (GEO) database and analyzed them by using GEO2R. Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes were used for the functional and pathway enrichment analysis. We constructed the protein-protein interaction (PPI) network by STRING and visualized it by Cytoscape. Further, we performed module analysis and centrality analysis to find the potential key genes. Finally, we carried on survival analysis of key genes by GEPIA.
resultsIn total, we obtained 685 DEGs. Moreover, GO analysis showed that they were mainly enriched in cell adhesion, proteinaceous extracellular region, heparin binding. KEGG pathway analysis revealed that transcriptional misregulation in cancer, ECM-receptor interaction, cell cycle and p53 signaling pathway were involved in. Furthermore, PPI network was constructed including 249 nodes and 1,027 edges. Additionally, a significant module was found, which included eight candidate genes with high centrality features. Further, among the eight candidate genes, the survival of NSCLC patients with the seven high expression genes were significantly worse, including CDK1, CCNB1, CCNA2, BIRC5, CCNB2, KIAA0101 and MELK. In summary, these identified genes should play an important role in NSCLC, which can provide new insight for NSCLC research.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.