همایش ملی بیوانفورماتیک ایران

صفحه اصلی / 4th international edition and 13th Iranian Conference on Bioinformatics

Dissecting the impact of smoking on epigenetic mechanisms that influencing Lung cancer susceptibility

نویسندگان :

Mahboobeh Golchinpour¹ Alireza Fotuhi Siahpirani²

1- Laboratory of Bioinformatics and Computational Genomics (LBCG), Department of Bioinformatics, Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran 2- Laboratory of Bioinformatics and Computational Genomics (LBCG), Department of Bioinformatics, Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran

کلمات کلیدی :

Gene Regulation،lung cancer susceptibility،differentially accessible regions

چکیده :

Epigenetic mechanisms play a crucial role in mediating the effects of environmental factors on cell fate and disease. One such environmental factor is smoking which is a major risk factor in lung cancer. To assess how smoking affect lung cancer susceptibility, we used a publicly available dataset (GSE241468), which examines the epigenetic landscapes and gene regulation in human lung cells by using multiome (transcriptome and chromatin accessibility) maps from 117,911 lung cells derived from 4 males and 4 females in each group of smokers and never-smokers (Long et al. 2024). Here, we reanalyzed this dataset, to identify differentially accessible regions (DARs) and differentially expressed genes (DEGs) between smokers and never-smokers. Seurat and Signac were used for preprocessing of the dataset. We then used a correlation-based approach for identifying candidate CREs in DARs and showed enrichment of binding motifs of transcription factors that are activated in these regions in response to smoking. By characterizing cell-type-specific CREs, our analysis showed that smoking-responsive genes predominantly exhibit cell-type-specific differential expression which contribute to lung cancer susceptibility. Results suggests that DARs contribute to augmented transcriptional responses under smoking conditions and affect lung cancer susceptibility. By linking these epigenetic alterations directly to smoking and identifying key target genes and cell types, our findings provide a map of the epigenetic landscape shaping lung cancer risk and open avenues for targeted interventions in these epigenetically altered pathways.

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