| description |
Cancer cells carry various types of aberrations at the levels of genome, epigenome and transcriptome. For future studies on the biological relevance of the aberrations and their mutual relations, we generated a multi-omics catalogue of 26 lung adenocarcinoma cell lines. By whole-genome sequencing, we detected SNVs and indels, copy number aberrations and chromosome rearrangements. We used RNA-Seq to examine whether those mutation-harboring genes are expressed in the corresponding cell lines or whether their expression levels are deviated between the cell lines. Also, we could detect known and novel abnormal transcripts, such as RET- and ALK-fusion transcripts and transcripts caused by splice site mutations. Similarly, target-captured bisulfite sequencing and ChIP-Seq analyses revealed epigenomic status in each cell line and their deviations. We integrated these multi-omics data to explain possible causes of the observed aberrant gene expressions, particular for the representative cancer-related genes. We unexpectedly found that the patterns of aberrations were highly diverse between genes; namely irregular chromatin status revealed by ChIP-Seq was the characteristic to the EGFR, while a large genomic deletion and hyper-DNA methylation in the promoter region were the most frequent for the CDKN2A gene. Our datasets, by complementing current whole-exome or whole-genome sequencing of clinical cancers, should lay valuable base for interpreting how various types of genomic and epigenomic aberration lead to aberrant transcriptomic appearances in cancers. |