ArticleCarcinogenesis2019
Systematic analyses of regulatory variants in DNase I hypersensitive sites identified two novel lung cancer susceptibility loci.
Article in Carcinogenesis, 2019. 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, 8 citations in OpenAlex.
- SLC16A1 Activates the STAT3/SLC7A11 Pathway to Mediate Ferroptosis Resistance and Tumor Progression in Head and Neck Squamous Cell Carcinoma.Oncology research · 2026Article
- SLC16A1 Inhibits Ferroptosis and Promotes the Progression of Head and Neck Squamous Cell Carcinoma.Journal of Cancer · 2025Article
- Development and validation of a chromatin regulator signature for predicting prognosis hepatocellular carcinoma patient.Journal of gastrointestinal oncology · 2024Article
- The Pivotal Function of SLC16A1 and SLC16A1-AS1 in Cancer Progress: Molecular Pathogenesis and Prognosis.Mini reviews in medicinal chemistry · 2024Article
- MRGBP: A New Factor for Diagnosis and Prediction of Head and Neck Squamous Cell Carcinoma.BioMed research international · 2022Article
- Prognostic Value and Immunological Role of MORF4-Related Gene-Binding Protein in Human Cancers.Frontiers in cell and developmental biology · 2021Article
- Association Analysis of Driver Gene-Related Genetic Variants Identified Novel Lung Cancer Susceptibility Loci with 20,871 Lung Cancer Cases and 15,971 Controls.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020Article
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Authors and funding
37 authors at 20 institutions in 12 countries.
Funding
Abstract
DNase I hypersensitive sites (DHS) are abundant in regulatory elements, such as promoter, enhancer and transcription factor binding sites. Many studies have revealed that disease-associated variants were concentrated in DHS-related regions. However, limited studies are available on the roles of DHS-related variants in lung cancer. In this study, we performed a large-scale case-control study with 20 871 lung cancer cases and 15 971 controls to evaluate the associations between regulatory genetic variants in DHS and lung cancer susceptibility. The expression quantitative trait loci (eQTL) analysis and pathway-enrichment analysis were performed to identify the possible target genes and pathways. In addition, we performed motif-based analysis to explore the lung-cancer-related motifs using sequence kernel association test. Two novel variants, rs186332 in 20q13.3 (C>T, odds ratio [OR] = 1.17, 95% confidence interval [95% CI]: 1.10-1.24, P = 8.45 × 10-7) and rs4839323 in 1p13.2 (T>C, OR = 0.92, 95% CI: 0.89-0.95, P = 1.02 × 10-6) showed significant association with lung cancer risk. The eQTL analysis suggested that these two SNPs might regulate the expression of MRGBP and SLC16A1, respectively. What's more, the expression of both MRGBP and SLC16A1 was aberrantly elevated in lung tumor tissues. The motif-based analysis identified 10 motifs related to the risk of lung cancer (P < 1.71 × 10-4). Our findings suggested that variants in DHS might modify lung cancer susceptibility through regulating the expression of surrounding genes. This study provided us a deeper insight into the roles of DHS-related genetic variants for lung cancer.
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