Hi-ChIP dataset for epigenomics landscape of colorectal cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA562895 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10043495_1.fastq.gz | Fastqsanger.gz | |||
| SRR10043495_2.fastq.gz | Fastqsanger.gz | |||
| SRR10043496_1.fastq.gz | Fastqsanger.gz | |||
| SRR10043496_2.fastq.gz | Fastqsanger.gz | |||
| SRR10043497_1.fastq.gz | Fastqsanger.gz |
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Project description:Cancer cells utilize genetic and epigenetic aberrations for their excessive growth. Although we have sufficient understanding of the genomic alterations in colorectal cancer, we have incomplete knowledge of epigenomic aberrations and their impact on tumor growth. In order to comprehensively define the epigenetic patterns specific to colorectal cancer, we generated profiles for 6 histone modification marks, including H3K4me1 (enhancer), H3K27Ac (active enhancer), H3K9me3 (heterochromatin), H3K27me3 (polycomb repression), H3K79me2 (transcription) and H3K4me3 (promoter), using a high-throughput ChIP-Seq methodology developed in house applicable to frozen tumors. Chromatin state transitions specifically pointed to drastic changes in enhancer patterns, consistent with some prior studies. Furthermore, we identified the best combinatorial chromatin states that could most efficiently distinguish and predict CRC from normal colon. In a more detailed investigation into patterns of active enhancers using normal colon, adenomas and colorectal cancers, we identified specific changes in enhancers from normal tissue to these neoplastic lesions. Importantly, we noted gains of enhancers in a large number of genomic loci in colon cancer compared to adjacent normal tissues. In summary, we have identified aberrant enhancer gains as a major feature of colorectal cancer and propose this to be utilized as a therapeutic approach.
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