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Targeting the vulnerability of arachidonic acid metabolism to enhance immunotherapy efficacy in ARID1A-deficient colorectal cancer [ChIP-Seq]

GSE278082 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2024/11/26 Platform GPL24247
Summary
ARID1A, a core constituent of SWI/SNF complex, is mutated in about 10% of colorectal cancer (CRC). This study demonstrates a synergistic effect of arachidonic acid metabolism inhibitors with immune checkpoint inhibitors (ICIs) by regulating functionality of CD8+ T cells and vasculogenic mimicry (VM) formation in ARID1A-deficient CRC. Mechanistically, ATAC-seq and ChIP-qPCR demonstrated that the lack of ARID1A results in reduced levels of the key enzymes PTGS1 and PTGS2, which control the arachidonic acid pathway. This reduction generated a reliance on the remaining functionality of arachidonic acid pathway in ARID1A-deficient cells.
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Direct links to NCBI, no account and no request form: the whole study as GSE278082_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 8 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1165662 and SRA study SRP534955. Searching any of these in the dataset finder brings you back here.

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