Abstract 373P
Background
Considerable differences in molecular characteristics have been defined between non-smokers and smokers in patients with lung adenocarcinoma (LUAD). However, study of open chromatin patterns associated with LUAD progression caused by smoking is still lacking.
Methods
Here, we firstly constructed a novel network based on correlations between each ATAC-seq peak from TCGA data using our previously developed algorithm. Subsequently, principal component analysis was performed on LUAD samples with retained peaks filtered by the correlation network. Prognostic value of the significant ATAC-seq peak set with overall survival in these smoking related LUAD patients was assessed. Then, pathway analysis of the peak-related genes was conducted for potential pathways identification.
Results
We identified a set of peaks with significant correlation that clearly differentiated long-term smokers from those with short-term smoking history in LUAD patients and also significantly associated with overall survival of these patients. The gene set that were demonstrated to be related to those peaks, such as B3GNT3, ACTN4 and CLDN3, are strongly associated with LUAD development, which is consistent with the important roles for the associated pathways in LUAD oncogenesis induced by smoking, including glycosphingolipid biosynthesis and tight junction pathways.
Conclusions
Our study may provide valuable insights on exploration of ATAC-seq peaks and on smoking-related LUAD carcinogenesis from a perspective of open chromatin changes.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
BGI-Shenzhen, Shenzhen 518083, China.
Funding
Science, Technology, and Innovation Commission of Shenzhen Municipality.
Disclosure
All authors have declared no conflicts of interest.
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